A high-fat diet may not always pack on the pounds, new research from the Warren Alpert Medical School suggests. By successfully preventing weight gain in mice, researchers have shed light on obesity prevention in humans. The study was released online last week and will be published in the January 2012 issue of Endocrinology, a science journal.
Even though the mice were on a high-fat diet, researchers were able to significantly reduce their weight gain by activating a human enzyme called IKKbeta in their fatty tissue. The enzyme normally triggers immune responses, such as inflammation, following increases in the number of human fat cells.
Researchers were curious to see what would happen if they reversed the order of events by activating the enzyme prior to weight gain.
They found that in addition to reduced weight gain, the mice with the activated enzyme also had faster metabolisms. In these mice, insulin was more effective at lowering blood sugar than it was in the mice that had not been treated.
The activated enzyme also inhibited resistance to insulin, another side effect of obesity.
The study has definite implications for helping people who suffer from conditions characterized by insulin resistance, such as Type 2 diabetes patients, said Haiyan Xu, assistant professor of medicine...
Saturday, December 17, 2011
New Weight-Loss Drug Reduces Body Weight in Monkeys, Mice
Researchers at the University of Texas MD Anderson Cancer Center have developed a drug that assaults the blood supply of fat cells and led to weight loss in obese rhesus monkeys.
Renata Pasqualini, Ph.D., co-senior author of the study and professor in MD Anderson's David H. Koch Center for Applied Research for Genitourinary Cancers, along with Wadih Arap, M.D., co-senior author of the study and a professor in the Koch Center, and Kirstin Barnhart, D.V.M., Ph.D., veterinary clinical pathologist at MD Anderson's Keeling Center for Comparative Medicine and Research, have created a new weight-loss drug that could potentially reduce accumulated white fat in humans.
Currently, weight-loss drugs work to suppress the appetite or increase metabolism in order to combat obesity, but harmful side effects come with the use of such drugs.
Now, Pasqualini and Arap have designed a new drug called Adipotide, which attacks white adipose tissue. This tissue is an unhealthy kind of fat that accumulates around the abdomen and under the skin. Adipotide contains a homing agent that attaches to a protein on the surface of blood vessels that support the fat. A synthetic peptide then triggers cell death, and with a lack of blood supply, the fat cells are reabsorbed.
The drug was used in mice models and rhesus monkey models. Adipotide was able to decrease abdominal circumference, body mass index (BMI) and body fat.
According to the study, the obese mice lost about 30 percent of their body weight while on Adipotide. The rhesus monkeys in the study, which were "spontaneously" obese due to overeating and a lack of physical activity, had a 27 percent decrease in abdominal fat levels. The drug reduced the weight of rhesus monkeys by 11 percent in just one month...
Renata Pasqualini, Ph.D., co-senior author of the study and professor in MD Anderson's David H. Koch Center for Applied Research for Genitourinary Cancers, along with Wadih Arap, M.D., co-senior author of the study and a professor in the Koch Center, and Kirstin Barnhart, D.V.M., Ph.D., veterinary clinical pathologist at MD Anderson's Keeling Center for Comparative Medicine and Research, have created a new weight-loss drug that could potentially reduce accumulated white fat in humans.
Currently, weight-loss drugs work to suppress the appetite or increase metabolism in order to combat obesity, but harmful side effects come with the use of such drugs.
Now, Pasqualini and Arap have designed a new drug called Adipotide, which attacks white adipose tissue. This tissue is an unhealthy kind of fat that accumulates around the abdomen and under the skin. Adipotide contains a homing agent that attaches to a protein on the surface of blood vessels that support the fat. A synthetic peptide then triggers cell death, and with a lack of blood supply, the fat cells are reabsorbed.
The drug was used in mice models and rhesus monkey models. Adipotide was able to decrease abdominal circumference, body mass index (BMI) and body fat.
According to the study, the obese mice lost about 30 percent of their body weight while on Adipotide. The rhesus monkeys in the study, which were "spontaneously" obese due to overeating and a lack of physical activity, had a 27 percent decrease in abdominal fat levels. The drug reduced the weight of rhesus monkeys by 11 percent in just one month...
Scripps Research scientists uncover new role for gene in maintaining steady weight
Against the backdrop of the growing epidemic of obesity in the United States, scientists from the Florida campus of The Scripps Research Institute have made an important new discovery regarding a specific gene that plays an important role in keeping a steady balance between our food intake and energy expenditure. The study may help scientists better understand the keys to fighting obesity and related disorders such as diabetes. The study, which was published in the November 25, 2011 print edition of The Journal of Biological Chemistry, focused on the melanocortin-3 receptor (MC3R), which normally responds to signals of nutrient intake.
"What we discovered was quite a surprise," said Scripps Research Associate Professor Andrew Butler, who led the study. "We thought that the actions of the receptor expressed in the brain would be critical for metabolic homeostasis. However, what we found is that actions of the receptor expressed outside the brain appear to be equally important."
The existence of drug targets in areas outside of the central nervous system (the body's "periphery") might help in the effort to develop drugs that influence metabolism without major side effects, Butler said.
The findings were made possible by the team's development of a new transgenic animal model, where expression of the MC3R gene can be selectively "switched on" in different cell types.
In the study, the suppression of MC3R expression in the brain and peripheral tissues had a marked impact on metabolic homeostasis (equilibrium). Interestingly, mice expressing the MC3R gene in the brain only displayed an obese phenotype (physical appearance) similar to those where all types of expression was suppressed, indicating that actions of this receptor in the brain are not sufficient to protect against weight gain.
"What we discovered was quite a surprise," said Scripps Research Associate Professor Andrew Butler, who led the study. "We thought that the actions of the receptor expressed in the brain would be critical for metabolic homeostasis. However, what we found is that actions of the receptor expressed outside the brain appear to be equally important."
The existence of drug targets in areas outside of the central nervous system (the body's "periphery") might help in the effort to develop drugs that influence metabolism without major side effects, Butler said.
The findings were made possible by the team's development of a new transgenic animal model, where expression of the MC3R gene can be selectively "switched on" in different cell types.
In the study, the suppression of MC3R expression in the brain and peripheral tissues had a marked impact on metabolic homeostasis (equilibrium). Interestingly, mice expressing the MC3R gene in the brain only displayed an obese phenotype (physical appearance) similar to those where all types of expression was suppressed, indicating that actions of this receptor in the brain are not sufficient to protect against weight gain.
Neuron Transplant Reduces Obesity In Mice
Scientists at Harvard University have successfully transplanted neurons into the brains of obesity-prone mice to prevent them from getting fat. The researchers did not have human obesity in mind when conducting the experiment; rather, they used the neuron transplant as an example of a method to restore function to abnormal neural circuits. The results have highlighted the promise in cell therapies. For example, scientists could soon transplant stem cells or fetal cells to treat nervous system diseases.
Throughout the years, research on cell therapies has rarely found success. Experiments using stem cell therapy to treat spinal injuries as well as some trials involving fetal cell therapy for Parkinson’s disease have yielded no positive results. Only until recent years has it been proven that the human brain produces new neurons throughout the lifetime. Some evidence has shown that these new neurons are occasionally integrated into existing neural circuits and actually enhance brain function. This evidence led scientists to postulate that this could be done using transplanted cells as well.
Obesity prone mice were used to test a special fetal stem cell therapy. | Photo courtesy of Bigplankton via Wikimedia Commons
The Harvard University scientists extracted healthy neurons from mouse embryos (the hypothalamus to be exact) and transplanted those neurons into the same region of the brain in obesity prone mice. These mice lack the receptor for leptin, a hormone that regulates metabolism and body weight, and therefore they are prone to being diabetic and obese. The transplanted neurons were labeled with a green fluorescent protein to track them in the neural circuit. The results were quite promising, as the transplanted neurons were able to integrate efficiently into the existing neural circuit and develop into mature neurons that responded to leptin. At the end of the experiment, the treated mice weighed 30% less than mice that had not received a transplant. This suggested that the transplanted neurons actually fixed the damaged neural circuit.
Though the experiment was not directed towards treating human obesity, the success of the experiment gave scientists a light at the end of the tunnel in terms of cell therapies...
Throughout the years, research on cell therapies has rarely found success. Experiments using stem cell therapy to treat spinal injuries as well as some trials involving fetal cell therapy for Parkinson’s disease have yielded no positive results. Only until recent years has it been proven that the human brain produces new neurons throughout the lifetime. Some evidence has shown that these new neurons are occasionally integrated into existing neural circuits and actually enhance brain function. This evidence led scientists to postulate that this could be done using transplanted cells as well.
Obesity prone mice were used to test a special fetal stem cell therapy. | Photo courtesy of Bigplankton via Wikimedia Commons
The Harvard University scientists extracted healthy neurons from mouse embryos (the hypothalamus to be exact) and transplanted those neurons into the same region of the brain in obesity prone mice. These mice lack the receptor for leptin, a hormone that regulates metabolism and body weight, and therefore they are prone to being diabetic and obese. The transplanted neurons were labeled with a green fluorescent protein to track them in the neural circuit. The results were quite promising, as the transplanted neurons were able to integrate efficiently into the existing neural circuit and develop into mature neurons that responded to leptin. At the end of the experiment, the treated mice weighed 30% less than mice that had not received a transplant. This suggested that the transplanted neurons actually fixed the damaged neural circuit.
Though the experiment was not directed towards treating human obesity, the success of the experiment gave scientists a light at the end of the tunnel in terms of cell therapies...
Weight-Loss Enzyme Identified by Brown Researchers
While not the solution to holiday weight gain, a new study from Brown University researchers sheds promising new light on metabolism and weight loss.
Scientists report that they substantially curbed weight gain, improved metabolism, and improved the efficacy of insulin in mice by engineering them to express a specific human enzyme in their fat tissue. Although the obesity prevention came at the significant cost of widespread inflammation, the research offers new clues about the connections among obesity, insulin resistance and type 2 diabetes, and inflammation...
Scientists report that they substantially curbed weight gain, improved metabolism, and improved the efficacy of insulin in mice by engineering them to express a specific human enzyme in their fat tissue. Although the obesity prevention came at the significant cost of widespread inflammation, the research offers new clues about the connections among obesity, insulin resistance and type 2 diabetes, and inflammation...
Cilia control eating signal
The action of tiny hairlike appendages on cells can mean the difference between fat and thin. Now scientists have a better idea of how the little hairs, called primary cilia, control appetite.
Primary cilia — single, hairlike projections that all cells in vertebrates usually have — seem to sequester a protein that senses and responds to an appetite-stimulating hormone, Nicolas Berbari of the University of Alabama at Birmingham reported December 6 at the annual meeting of the American Society for Cell Biology. In people and mice that lack primary cilia, the appetite stimulant works overtime, leading to overeating and obesity, Berbari said.
These findings may lead to new ways to control appetite and prevent or reverse obesity.
And the study may help scientists better understand the process of eating, said Kirk Mykytyn, a cell biologist at Ohio State University in Columbus. “This work is important because it’s more thoroughly clarifying the molecular mechanism involved in obesity associated with the loss of cilia,” he said...
Primary cilia — single, hairlike projections that all cells in vertebrates usually have — seem to sequester a protein that senses and responds to an appetite-stimulating hormone, Nicolas Berbari of the University of Alabama at Birmingham reported December 6 at the annual meeting of the American Society for Cell Biology. In people and mice that lack primary cilia, the appetite stimulant works overtime, leading to overeating and obesity, Berbari said.
These findings may lead to new ways to control appetite and prevent or reverse obesity.
And the study may help scientists better understand the process of eating, said Kirk Mykytyn, a cell biologist at Ohio State University in Columbus. “This work is important because it’s more thoroughly clarifying the molecular mechanism involved in obesity associated with the loss of cilia,” he said...
Saturday, November 26, 2011
Neuron Transplants Can Repair Brain Circuits
A new study by Harvard University neuroscientist Jeffrey Macklis and colleagues suggests it is possible to transplant fetal neurons into a part of the mouse brain that does not normally generate new brain cells, and they will repair abnormal circuits. In this case, the researchers repaired a genetic defect that causes obesity, but that was not the goal of their work which was to establish proof of principle that transplanted neurons can integrate into existing faulty brain circuits and restore them...
Sunday, November 20, 2011
New Weight-Loss Drug Reduces Body Weight in Monkeys, Mice
The new drug, called Adipotide, attacks white adipose tissue under the skin and around the abdomen
Researchers at the University of Texas MD Anderson Cancer Center have developed a drug that assaults the blood supply of fat cells and led to weight loss in obese rhesus monkeys.
Renata Pasqualini, Ph.D., co-senior author of the study and professor in MD Anderson's David H. Koch Center for Applied Research for Genitourinary Cancers, along with Wadih Arap, M.D., co-senior author of the study and a professor in the Koch Center, and Kirstin Barnhart, D.V.M., Ph.D., veterinary clinical pathologist at MD Anderson's Keeling Center for Comparative Medicine and Research, have created a new weight-loss drug that could potentially reduce accumulated white fat in humans.
Currently, weight-loss drugs work to suppress the appetite or increase metabolism in order to combat obesity, but harmful side effects come with the use of such drugs.
Now, Pasqualini and Arap have designed a new drug called Adipotide, which attacks white adipose tissue. This tissue is an unhealthy kind of fat that accumulates around the abdomen and under the skin. Adipotide contains a homing agent that attaches to a protein on the surface of blood vessels that support the fat. A synthetic peptide then triggers cell death, and with a lack of blood supply, the fat cells are reabsorbed.
The drug was used in mice models and rhesus monkey models. Adipotide was able to decrease abdominal circumference, body mass index (BMI) and body fat...
Researchers at the University of Texas MD Anderson Cancer Center have developed a drug that assaults the blood supply of fat cells and led to weight loss in obese rhesus monkeys.
Renata Pasqualini, Ph.D., co-senior author of the study and professor in MD Anderson's David H. Koch Center for Applied Research for Genitourinary Cancers, along with Wadih Arap, M.D., co-senior author of the study and a professor in the Koch Center, and Kirstin Barnhart, D.V.M., Ph.D., veterinary clinical pathologist at MD Anderson's Keeling Center for Comparative Medicine and Research, have created a new weight-loss drug that could potentially reduce accumulated white fat in humans.
Currently, weight-loss drugs work to suppress the appetite or increase metabolism in order to combat obesity, but harmful side effects come with the use of such drugs.
Now, Pasqualini and Arap have designed a new drug called Adipotide, which attacks white adipose tissue. This tissue is an unhealthy kind of fat that accumulates around the abdomen and under the skin. Adipotide contains a homing agent that attaches to a protein on the surface of blood vessels that support the fat. A synthetic peptide then triggers cell death, and with a lack of blood supply, the fat cells are reabsorbed.
The drug was used in mice models and rhesus monkey models. Adipotide was able to decrease abdominal circumference, body mass index (BMI) and body fat...
A specific human enzyme may help tackle obesity and diabetes, if a new scientific report is to be believed.
In a new study, scientists have reported that they substantially curbed weight gain, improved metabolism, and improved the efficacy of insulin in mice by engineering them to express a specific human enzyme in their fat tissue.
Although the obesity prevention came at the significant cost of widespread inflammation, the research offers new clues about the connections among obesity, insulin resistance and type 2 diabetes, and inflammation.
"Turning on this molecule has a very dramatic impact on lipid metabolism," said Haiyan Xu, assistant professor of medicine (research) in the Warren Alpert Medical School of Brown University and a researcher at Rhode Island Hospital's Hallett Center for Diabetes and Endocrinology.
In the study, the researchers changed the sequence of events for transgenically engineered mice by inducing inflammation via the enzyme IKKbeta in their fatty tissue before they were obese. The result for metabolism was much more positive than for control mice who were left unaltered but were fed the same diets...
In a new study, scientists have reported that they substantially curbed weight gain, improved metabolism, and improved the efficacy of insulin in mice by engineering them to express a specific human enzyme in their fat tissue.
Although the obesity prevention came at the significant cost of widespread inflammation, the research offers new clues about the connections among obesity, insulin resistance and type 2 diabetes, and inflammation.
"Turning on this molecule has a very dramatic impact on lipid metabolism," said Haiyan Xu, assistant professor of medicine (research) in the Warren Alpert Medical School of Brown University and a researcher at Rhode Island Hospital's Hallett Center for Diabetes and Endocrinology.
In the study, the researchers changed the sequence of events for transgenically engineered mice by inducing inflammation via the enzyme IKKbeta in their fatty tissue before they were obese. The result for metabolism was much more positive than for control mice who were left unaltered but were fed the same diets...
Thursday, November 17, 2011
Metabolism Boosted By Enzyme, Weight Gain Prevented In Mice
Male and female mice engineered to express the inflammatory enzyme IKKbeta in their fat tissue ate more but gained less weight. They burned sugar and fat more effectively than mice who were left unaltered. The research may shed light on how obesity and inflammation affect insulin resistance and sensitivity.
In a new study, scientists report that they substantially curbed weight gain, improved metabolism, and improved the efficacy of insulin in mice by engineering them to express a specific human enzyme in their fat tissue. Although the obesity prevention came at the significant cost of widespread inflammation, the research offers new clues about the connections among obesity, insulin resistance and type 2 diabetes, and inflammation...
In a new study, scientists report that they substantially curbed weight gain, improved metabolism, and improved the efficacy of insulin in mice by engineering them to express a specific human enzyme in their fat tissue. Although the obesity prevention came at the significant cost of widespread inflammation, the research offers new clues about the connections among obesity, insulin resistance and type 2 diabetes, and inflammation...
Sunday, November 13, 2011
Research Report: Hormone fights fat with fat
There are two types of body fat: white fat that stores energy and brown fat (packed with blood vessels and mitrochondria) that burns white fat. Long thought to disappear after infancy, brown fat has been rediscovered in adults humans using new imaging technology.
Sanford-Burnham Medical Research Institute researchers now report the discovery of orexin; a hormone that activates calorie-burning brown fat in mice. Orexin deficiency is associated with obesity, suggesting that supplemental orexin could lead to a new class of fat-fighting drugs focused on peripheral fat-burning tissue rather than the brain’s appetite control center which is the aim of most current weight-loss agents...
Sanford-Burnham Medical Research Institute researchers now report the discovery of orexin; a hormone that activates calorie-burning brown fat in mice. Orexin deficiency is associated with obesity, suggesting that supplemental orexin could lead to a new class of fat-fighting drugs focused on peripheral fat-burning tissue rather than the brain’s appetite control center which is the aim of most current weight-loss agents...
Microbes may be key to good health
Consider this: The average person's body contains about 100 trillion cells, but only maybe one in 10 is human.
This isn't the latest Hollywood horror flick, or some secret genetic engineering experiment run amok.
This, it turns out, is nature's way: The human cells that form our skin, eyes, ears, brain and every other part of our bodies are far outnumbered by those from microbes, primarily bacteria but also viruses, fungi and a panoply of other microorganisms.
That thought might make a lot of people lunge for the hand sanitizer, at the least. But that predictable impulse may be exactly the wrong one. A growing body of evidence indicates that the microbial ecosystems that have long populated our guts, mouths, noses and every other nook and cranny play crucial roles in keeping us healthy.
Moreover, researchers are becoming more convinced that modern trends -- diet, antibiotics, obsession with cleanliness, Caesarean delivery of babies --- are disrupting this delicate balance, contributing to some of the most perplexing ailments, including asthma, allergies, obesity, diabetes, autoimmune diseases, cancer and perhaps even autism.
"In terms of potential for human health, I would place it with stem cells as one of the two most promising areas of research at the moment," said Rob Knight of the University of Colorado. "Everywhere we look, microbes seem to be involved."
Equipped with super-fast new DNA decoders, scientists are accelerating the exploration of this realm at a molecular level, yielding provocative insights into how these microbial stowaways may wield far greater powers than previously appreciated in, paradoxically, making us human.
"The field has exploded," said Jeffrey Gordon of Washington University, who pioneered the exploration of humanity's microbial inhabitants, known as the "microbiome" or "microbiota." "People have this sense of wonderment about looking at themselves as a compilation of microbial and human parts."
Some equate these microbial inhabitants to a newly recognized organ. Acquired beginning at birth, this mass of fellow travelers may help steer normal development, molding immune systems and calibrating fundamental metabolic functions such as energy storage and consumption. There are even tantalizing clues they may help shape brain development, influencing behavior.
"The 'human supraorganism' is one term coined to describe the human host and all the attendant microorganisms," said Lita Proctor, who leads the Human Microbiome Project at the National Institutes of Health, which is mapping this world. "There's been a real revolution in thinking about what that means."
Investigators are trying to identify which organisms may truly be beneficial "probiotics" that people could take to help their health. Others are finding substances that people might ingest to nurture the good bugs. Drugs may mimic the helpful compounds that these organisms produce.
Doctors have even begun microbiota "transplants" to treat a host of illnesses, including a sometimes-devastating gastrointestinal infection called C. difficile, digestive system ailments such as Crohn's disease, colitis and irritable bowel disorder, and even in a handful of cases obesity and other afflictions, such as multiple sclerosis.
Many advocates of the research urge caution, noting that most of the work so far has involved laboratory animals or small numbers of patients, many hypotheses remain far from proven and nothing has zero risk.
"We have to be very careful in how we state what we know at the present time versus what we think might be true at this point," said David Relman of Stanford University. "But it's probably fair to say that our indigenous communities are more diverse, more complex and more intimately and intricately involved in our biology than we thought."
Scientists have long known that many organisms evolved with humans and perform vital functions, digesting food, extracting crucial nutrients, fighting off disease-causing entities.
But as microbiologists have begun scrutinizing these colonies, it has become clearer that they create carefully calibrated enterprises, with unique combinations inhabiting individual crevices and identifiable nuances from person to person.
European scientists reported in April that people generally seem to have one of three basic combinations that may be as fundamentally important as, say, blood type.
The five-year, $175 million U.S. Human Microbiome Project is assembling an outline of a "healthy" microbiome by sampling the mouth, airway, skin, gut and urogenital tract of 300 healthy adults, as well as deciphering the genetic codes of 200 possibly key microbes.
Dozens of studies are also underway, including some that are repeatedly swabbing kids and adults, including twins, to gain insights into why one person gets tooth decay, asthma, ulcerative colitis or even cancer, and another doesn't.
One intriguing finding is that babies born through Caesarean sections apparently miss out on acquiring their mothers' microbiota.
"The birth canal is very heavily colonized by bacteria," said Maria Dominguez-Bello, a University of Puerto Rico biologist who has been studying microbiota around the world, including in isolated tribes in the Amazon. "We think that is not by chance."
The interaction between the microbiota and the immune system may also play a role in other diseases in adults, including those caused at least in part by chronic inflammation from hyperactive immune systems.
"Gut bacteria have figured out a way to network with our immune system so it doesn't attack them," said Sarkis Mazmanian of the California Institute of Technology.
The microbiota apparently sends signals that dampen the "inflammatory response," a crucial defense also believed to play a role in a variety of diseases, including many forms of cancer, the "metabolic syndrome" caused by obesity, diabetes and heart disease.
The theory is that one reason some people may be prone to these diseases is that they are missing certain microbes. One anti-inflammatory compound produced by a bacterium appears to cure the equivalent of colitis and multiple sclerosis in mice, both of which are caused by misfiring immune systems, Mazmanian found.
Similarly, studies indicate that gut dwellers secrete messengers to cells lining the digestive tract to modulate key hormones, such as leptin and ghrelin, which are players in regulating metabolism, hunger and a sense of fullness.
Obese people appear to have a distinctive mix of digestive bacteria that make them prone to weight gain. Thin mice get fatter when their microbiota is replaced with the microbes of obese animals.
"Our ancient microbiome is losing the equilibrium it used to have with the host -- us -- and that has profound physiological consequences," said Martin Blaser of the New York University School of Medicine, who published his concerns in an August paper in the journal Nature.
Intriguing clues are also emerging about how microbes may affect the brain. Manipulating gut microbiomes of mice influences their anxiety and activity, Swedish researchers reported in January in the Proceedings of the National Academy of Sciences...
This isn't the latest Hollywood horror flick, or some secret genetic engineering experiment run amok.
This, it turns out, is nature's way: The human cells that form our skin, eyes, ears, brain and every other part of our bodies are far outnumbered by those from microbes, primarily bacteria but also viruses, fungi and a panoply of other microorganisms.
That thought might make a lot of people lunge for the hand sanitizer, at the least. But that predictable impulse may be exactly the wrong one. A growing body of evidence indicates that the microbial ecosystems that have long populated our guts, mouths, noses and every other nook and cranny play crucial roles in keeping us healthy.
Moreover, researchers are becoming more convinced that modern trends -- diet, antibiotics, obsession with cleanliness, Caesarean delivery of babies --- are disrupting this delicate balance, contributing to some of the most perplexing ailments, including asthma, allergies, obesity, diabetes, autoimmune diseases, cancer and perhaps even autism.
"In terms of potential for human health, I would place it with stem cells as one of the two most promising areas of research at the moment," said Rob Knight of the University of Colorado. "Everywhere we look, microbes seem to be involved."
Equipped with super-fast new DNA decoders, scientists are accelerating the exploration of this realm at a molecular level, yielding provocative insights into how these microbial stowaways may wield far greater powers than previously appreciated in, paradoxically, making us human.
"The field has exploded," said Jeffrey Gordon of Washington University, who pioneered the exploration of humanity's microbial inhabitants, known as the "microbiome" or "microbiota." "People have this sense of wonderment about looking at themselves as a compilation of microbial and human parts."
Some equate these microbial inhabitants to a newly recognized organ. Acquired beginning at birth, this mass of fellow travelers may help steer normal development, molding immune systems and calibrating fundamental metabolic functions such as energy storage and consumption. There are even tantalizing clues they may help shape brain development, influencing behavior.
"The 'human supraorganism' is one term coined to describe the human host and all the attendant microorganisms," said Lita Proctor, who leads the Human Microbiome Project at the National Institutes of Health, which is mapping this world. "There's been a real revolution in thinking about what that means."
Investigators are trying to identify which organisms may truly be beneficial "probiotics" that people could take to help their health. Others are finding substances that people might ingest to nurture the good bugs. Drugs may mimic the helpful compounds that these organisms produce.
Doctors have even begun microbiota "transplants" to treat a host of illnesses, including a sometimes-devastating gastrointestinal infection called C. difficile, digestive system ailments such as Crohn's disease, colitis and irritable bowel disorder, and even in a handful of cases obesity and other afflictions, such as multiple sclerosis.
Many advocates of the research urge caution, noting that most of the work so far has involved laboratory animals or small numbers of patients, many hypotheses remain far from proven and nothing has zero risk.
"We have to be very careful in how we state what we know at the present time versus what we think might be true at this point," said David Relman of Stanford University. "But it's probably fair to say that our indigenous communities are more diverse, more complex and more intimately and intricately involved in our biology than we thought."
Scientists have long known that many organisms evolved with humans and perform vital functions, digesting food, extracting crucial nutrients, fighting off disease-causing entities.
But as microbiologists have begun scrutinizing these colonies, it has become clearer that they create carefully calibrated enterprises, with unique combinations inhabiting individual crevices and identifiable nuances from person to person.
European scientists reported in April that people generally seem to have one of three basic combinations that may be as fundamentally important as, say, blood type.
The five-year, $175 million U.S. Human Microbiome Project is assembling an outline of a "healthy" microbiome by sampling the mouth, airway, skin, gut and urogenital tract of 300 healthy adults, as well as deciphering the genetic codes of 200 possibly key microbes.
Dozens of studies are also underway, including some that are repeatedly swabbing kids and adults, including twins, to gain insights into why one person gets tooth decay, asthma, ulcerative colitis or even cancer, and another doesn't.
One intriguing finding is that babies born through Caesarean sections apparently miss out on acquiring their mothers' microbiota.
"The birth canal is very heavily colonized by bacteria," said Maria Dominguez-Bello, a University of Puerto Rico biologist who has been studying microbiota around the world, including in isolated tribes in the Amazon. "We think that is not by chance."
The interaction between the microbiota and the immune system may also play a role in other diseases in adults, including those caused at least in part by chronic inflammation from hyperactive immune systems.
"Gut bacteria have figured out a way to network with our immune system so it doesn't attack them," said Sarkis Mazmanian of the California Institute of Technology.
The microbiota apparently sends signals that dampen the "inflammatory response," a crucial defense also believed to play a role in a variety of diseases, including many forms of cancer, the "metabolic syndrome" caused by obesity, diabetes and heart disease.
The theory is that one reason some people may be prone to these diseases is that they are missing certain microbes. One anti-inflammatory compound produced by a bacterium appears to cure the equivalent of colitis and multiple sclerosis in mice, both of which are caused by misfiring immune systems, Mazmanian found.
Similarly, studies indicate that gut dwellers secrete messengers to cells lining the digestive tract to modulate key hormones, such as leptin and ghrelin, which are players in regulating metabolism, hunger and a sense of fullness.
Obese people appear to have a distinctive mix of digestive bacteria that make them prone to weight gain. Thin mice get fatter when their microbiota is replaced with the microbes of obese animals.
"Our ancient microbiome is losing the equilibrium it used to have with the host -- us -- and that has profound physiological consequences," said Martin Blaser of the New York University School of Medicine, who published his concerns in an August paper in the journal Nature.
Intriguing clues are also emerging about how microbes may affect the brain. Manipulating gut microbiomes of mice influences their anxiety and activity, Swedish researchers reported in January in the Proceedings of the National Academy of Sciences...
Researchers Discover New Gene that Encodes for Diabetes Resistance
esearchers at the University of Wisconsin-Madison have identified a gene that may be responsible for determining an individual's susceptibility to both Type 1 and Type 2 diabetes. The study, which lasted over a decade, identified a gene in obese mice that controls a protein called tomosyn-2 - a compound responsible for decreased insulin production in pancreatic beta cells.
When insulin production in the pancreas is reduced diabetes can follow. Insulin is released into the bloodstream where it allows cells to absorb sugar and use it for energy. Individuals with Type 1 diabetes are insulin-deficient while those with Type 2 diabetes are insulin-resistant. Both forms of the disease cause significant complications, especially if it goes unmanaged.
The newly-discovered gene was found to affect insulin production in obese mice by reducing the activity of the protein tomosyn-2. While the gene can be controlled in mice, researchers will need to conduct further studies to determine whether medications that target the protein can be developed for humans.
"It's too early for us to know how relevant this gene will be to human diabetes, but the concept of negative regulation is one of the most interesting things to come out of this study and that very likely applies to humans," says Alan Attie, head of the study and biochemistry professor at University of Wisconsin-Madison.
The research team specifically used obese mice because they need more insulin to normalize blood glucose levels, especially after a meal, and humans have similar insulin needs. Being overweight requires more insulin to simply keep blood sugar levels regulated...
When insulin production in the pancreas is reduced diabetes can follow. Insulin is released into the bloodstream where it allows cells to absorb sugar and use it for energy. Individuals with Type 1 diabetes are insulin-deficient while those with Type 2 diabetes are insulin-resistant. Both forms of the disease cause significant complications, especially if it goes unmanaged.
The newly-discovered gene was found to affect insulin production in obese mice by reducing the activity of the protein tomosyn-2. While the gene can be controlled in mice, researchers will need to conduct further studies to determine whether medications that target the protein can be developed for humans.
"It's too early for us to know how relevant this gene will be to human diabetes, but the concept of negative regulation is one of the most interesting things to come out of this study and that very likely applies to humans," says Alan Attie, head of the study and biochemistry professor at University of Wisconsin-Madison.
The research team specifically used obese mice because they need more insulin to normalize blood glucose levels, especially after a meal, and humans have similar insulin needs. Being overweight requires more insulin to simply keep blood sugar levels regulated...
Estrogen Works in Brain To Regulate Female Weight
Estrogen regulates energy output, appetite and body weight, and insufficient estrogen receptors in certain regions of the brain may lead to obesity, according to a recent mouse study at the University of Texas Southwestern Medical Center.
“Estrogen has a profound effect on metabolism,” said Dr. Deborah Clegg, associate professor of internal medicine and senior author of the study. “We hadn’t previously thought of sex hormones as being critical regulators of food intake and body weight.”
The research is the first to demonstrate that estrogen works through two hypothalamic neural centers in the brain to regulate hunger and energy expenditure, keeping female body weight in check.
Female mice without the estrogen receptor alpha – a molecule that sends estrogen signals to neurons – in those parts of the brain became obese and developed related diseases, such as diabetes and heart disease.
These results were not replicated in male mice, although scientists believe other unknown estrogen receptor sites in the brain play a similar role in regulating male metabolism as well.
Although estrogen receptors are located throughout the body, researchers pinpointed two specific populations of estrogen receptors that seem to regulate energy balance for female mice...
“Estrogen has a profound effect on metabolism,” said Dr. Deborah Clegg, associate professor of internal medicine and senior author of the study. “We hadn’t previously thought of sex hormones as being critical regulators of food intake and body weight.”
The research is the first to demonstrate that estrogen works through two hypothalamic neural centers in the brain to regulate hunger and energy expenditure, keeping female body weight in check.
Female mice without the estrogen receptor alpha – a molecule that sends estrogen signals to neurons – in those parts of the brain became obese and developed related diseases, such as diabetes and heart disease.
These results were not replicated in male mice, although scientists believe other unknown estrogen receptor sites in the brain play a similar role in regulating male metabolism as well.
Although estrogen receptors are located throughout the body, researchers pinpointed two specific populations of estrogen receptors that seem to regulate energy balance for female mice...
Omega-3 key in reducing diabetes and heart disease
Omega-3 can help to reduce the risk of diabetes and heart disease especially as people age, says Massey University nutrition professor Bernhard Breier, co-author of a new international study.
Professor Breier, who leads an international research team, says omega-3s are especially beneficial for health in ageing because they improve carbohydrate and fat metabolism.
His research found a diet high in omega-3 fatty acids helps to burn metabolic fuels (glucose and fat) better, and can regulate energy storage across different tissues. This is despite genetic factors that predispose some people to gain weight more easily, making them potentially more susceptible to conditions such as diabetes and heart disease.
“These findings are important because the ageing process is closely linked with a higher risk of developing metabolic syndrome – a clustering of risk factors for heart disease, diabetes and obesity,” says Professor Breier, Chair of Human Nutrition at the Institute of Food, Nutrition and Human Health at Albany.
He says omega-3 fatty acids have been found to stimulate the process known as the insulin signalling cascade, which improves how blood sugar is used in the body. Researchers from Germany, Australia and New Zealand carried out tests on mice, examining the effects of feeding omega-3 rich diets to two groups with distinct, genetically determined traits to model different body types and metabolic responses of humans. One group developed obesity more easily and the second was a leaner variety.
When scientists measured changes to the metabolic responses, results showed the omega-3 rich diet reduced cholesterol and improved insulin action and fat metabolism in both groups of mice. However, the obesity prone mice responded less well than the leaner variety, drawing attention to genetically determined pathways that contribute to obesity...
Professor Breier, who leads an international research team, says omega-3s are especially beneficial for health in ageing because they improve carbohydrate and fat metabolism.
His research found a diet high in omega-3 fatty acids helps to burn metabolic fuels (glucose and fat) better, and can regulate energy storage across different tissues. This is despite genetic factors that predispose some people to gain weight more easily, making them potentially more susceptible to conditions such as diabetes and heart disease.
“These findings are important because the ageing process is closely linked with a higher risk of developing metabolic syndrome – a clustering of risk factors for heart disease, diabetes and obesity,” says Professor Breier, Chair of Human Nutrition at the Institute of Food, Nutrition and Human Health at Albany.
He says omega-3 fatty acids have been found to stimulate the process known as the insulin signalling cascade, which improves how blood sugar is used in the body. Researchers from Germany, Australia and New Zealand carried out tests on mice, examining the effects of feeding omega-3 rich diets to two groups with distinct, genetically determined traits to model different body types and metabolic responses of humans. One group developed obesity more easily and the second was a leaner variety.
When scientists measured changes to the metabolic responses, results showed the omega-3 rich diet reduced cholesterol and improved insulin action and fat metabolism in both groups of mice. However, the obesity prone mice responded less well than the leaner variety, drawing attention to genetically determined pathways that contribute to obesity...
Antibiotics Could Be Driving Up Obesity
The human gut is home to a galaxy of bacteria thought to protect us from disease in the digestive tract and beyond. So what happens when we take antibiotics?
Sure, the pills can wipe out bad bacteria. But they also kill the good stuff. On top of fueling a rise in antibiotic-resistant superbugs, they could be permanently changing the gut environment — a feat some experts fear might be making us fat.
Dr. Martin Blaser of New York University Langone Medical Center studies the effects of antibiotics on Helicobacter pylori — a bacterium that lives quietly in most but leads to ulcers in some.
Although the majority of H. pylori infections are harmless, doctors are quick to treat them with antibiotics that change the way the stomach works.
“Antibiotics are miraculous,” Blaser told ABCNews.com in August after publishing an editorial on antibiotic overuse. “They’ve changed health and medicine over the last 70 years. But when doctors prescribe antibiotics, it is based on the belief that there are no long-term effects. We’ve seen evidence that suggests antibiotics may permanently change the beneficial bacteria that we’re carrying.”
Blaser discussed his latest research with the New York Times, explaining that antibiotics for H. pylori trick the body into eating more by disrupting hunger hormone levels. Indeed, mice given antibiotics get fatter than their untreated counterparts despite having the same diet, Blaser said.
The findings add weight to studies that have found differences in gut bacteria between lean and obese mice. Changes in gut bacteria – called the microbiome – could also be a risk factor for allergies, asthma and diabetes...
Sure, the pills can wipe out bad bacteria. But they also kill the good stuff. On top of fueling a rise in antibiotic-resistant superbugs, they could be permanently changing the gut environment — a feat some experts fear might be making us fat.
Dr. Martin Blaser of New York University Langone Medical Center studies the effects of antibiotics on Helicobacter pylori — a bacterium that lives quietly in most but leads to ulcers in some.
Although the majority of H. pylori infections are harmless, doctors are quick to treat them with antibiotics that change the way the stomach works.
“Antibiotics are miraculous,” Blaser told ABCNews.com in August after publishing an editorial on antibiotic overuse. “They’ve changed health and medicine over the last 70 years. But when doctors prescribe antibiotics, it is based on the belief that there are no long-term effects. We’ve seen evidence that suggests antibiotics may permanently change the beneficial bacteria that we’re carrying.”
Blaser discussed his latest research with the New York Times, explaining that antibiotics for H. pylori trick the body into eating more by disrupting hunger hormone levels. Indeed, mice given antibiotics get fatter than their untreated counterparts despite having the same diet, Blaser said.
The findings add weight to studies that have found differences in gut bacteria between lean and obese mice. Changes in gut bacteria – called the microbiome – could also be a risk factor for allergies, asthma and diabetes...
Red wine has health benefits for obese men, study finds
For the first time, a study has proved that the active ingredient in red wine does make obese men significantly healthier.
“I was happily surprised with the findings,” lead author Patrick Schrauwen told the Star on Tuesday.
“The results were above expectations.”
After 30 days in a random, double-blind study, the obese men who were given 150 milligrams a day of resveratrol showed all the health benefits that come with a calorie-reduced diet and endurance training, Schrauwen said.
Their systolic blood pressure was lower, their mean arterial pressure fell, the fat levels in their livers and muscles dropped and their energy metabolism improved significantly, the study said.
Previous studies on mice showed health benefits from resveratrol, found in red wine and grapes...
“I was happily surprised with the findings,” lead author Patrick Schrauwen told the Star on Tuesday.
“The results were above expectations.”
After 30 days in a random, double-blind study, the obese men who were given 150 milligrams a day of resveratrol showed all the health benefits that come with a calorie-reduced diet and endurance training, Schrauwen said.
Their systolic blood pressure was lower, their mean arterial pressure fell, the fat levels in their livers and muscles dropped and their energy metabolism improved significantly, the study said.
Previous studies on mice showed health benefits from resveratrol, found in red wine and grapes...
Drug Devised to Reduce Obesity
Journal Science Translational Medicine published research has revealed that the US researchers have devised a drug, Adipotide, which has proved success among obese monkeys and mice.
Co-Lead researcher, Professor Renata Pasqualini was of the view that before experimenting drug on rhesus monkeys, they conducted experiment on obese mice. It was found that mice were able to lose 30% of their body weight.
It was only after the success of pre-clinical testing that they decided to have clinical test on rhesus monkeys. After the drug was given to them, it was found that they were able to reduce 11% of their body weight, and also reduced their increased waist line and their BMI also declined...
Co-Lead researcher, Professor Renata Pasqualini was of the view that before experimenting drug on rhesus monkeys, they conducted experiment on obese mice. It was found that mice were able to lose 30% of their body weight.
It was only after the success of pre-clinical testing that they decided to have clinical test on rhesus monkeys. After the drug was given to them, it was found that they were able to reduce 11% of their body weight, and also reduced their increased waist line and their BMI also declined...
Sunday, October 09, 2011
New study suggests inflammation may not be cause of obesity-type 2 diabetes link
For years, it has been assumed that obesity led to type 2 diabetes by causing inflammation, which was thought to change the way the body reacts to the effects of insulin. However, a new study suggests that this hypothesis may need an update.
Researchers from Children’s Hospital Boston reported in the journal Nature Medicine that inflammation actually activates two different proteins that play key roles in stablizing blood sugar levels. Without the presence of inflammation, these proteins remain dormant.
The findings suggest an important new role for inflammation in the body. Rather than being the cause of health problems like type 2 diabetes, heart disease and certain cancers, it may actually be a helpful reaction to other conditions in the body that are the real cause of disease...
Researchers from Children’s Hospital Boston reported in the journal Nature Medicine that inflammation actually activates two different proteins that play key roles in stablizing blood sugar levels. Without the presence of inflammation, these proteins remain dormant.
The findings suggest an important new role for inflammation in the body. Rather than being the cause of health problems like type 2 diabetes, heart disease and certain cancers, it may actually be a helpful reaction to other conditions in the body that are the real cause of disease...
Cold mice might be skewing weight-loss drug studies
Animals and people burn calories in an effort to keep warm, and room temperature may be affecting the testing and development of weight-loss drugs, says University of Alabama at Birmingham researcher Daniel Smith, Ph.D.
Smith, an instructor in the Department of Nutrition Sciences, received a 2011 Early-Career Research Grant from The Obesity Society for his proposal to examine the effect of room temperature on obesity-related drug effects in mice.
“More than 90 percent of weight-loss drugs that show promising results in lab tests fail to reach approval for treatment in humans,” said Smith. “There appears to be a translation gap from the bench to the market. I think the temperature used in animal research facilities may be part of the reason.”
Smith noted that most animals are tested in rooms where the temperature is near 22 degrees Celsius (72F), which is comfortable for most adult humans. However, that temperature is cold for mice, which have to eat more to elevate their metabolic rate to meet the constant, cold stress.
“If you raise the temperature to 30 degrees Celsius, that puts the mice in their thermo-neutral zone or a comfortable temperature for them, mimicking more closely what humans experience in modern daily life,” said Smith.
Smith will test a handful of weight-loss drugs in a group of mice housed at 22 degrees Celsius and another group at 30 degrees Celsius. Food intake, body weight and body composition will be measured to determine drug-related, weight-loss effects in the two temperatures. He said this study could be an important turning point for obesity researchers using animal models.
“This could change the models of pre-clinical drug testing,” said Smith...
Smith, an instructor in the Department of Nutrition Sciences, received a 2011 Early-Career Research Grant from The Obesity Society for his proposal to examine the effect of room temperature on obesity-related drug effects in mice.
“More than 90 percent of weight-loss drugs that show promising results in lab tests fail to reach approval for treatment in humans,” said Smith. “There appears to be a translation gap from the bench to the market. I think the temperature used in animal research facilities may be part of the reason.”
Smith noted that most animals are tested in rooms where the temperature is near 22 degrees Celsius (72F), which is comfortable for most adult humans. However, that temperature is cold for mice, which have to eat more to elevate their metabolic rate to meet the constant, cold stress.
“If you raise the temperature to 30 degrees Celsius, that puts the mice in their thermo-neutral zone or a comfortable temperature for them, mimicking more closely what humans experience in modern daily life,” said Smith.
Smith will test a handful of weight-loss drugs in a group of mice housed at 22 degrees Celsius and another group at 30 degrees Celsius. Food intake, body weight and body composition will be measured to determine drug-related, weight-loss effects in the two temperatures. He said this study could be an important turning point for obesity researchers using animal models.
“This could change the models of pre-clinical drug testing,” said Smith...
Parents' weight affects children, study shows
Overweight parents are more likely to have children who are obese which could lead to the need for weight loss surgery, according to a new study.
Thinner children are therefore more likely to come from slimmer families, researchers at University College London (UCL) have found through a national health survey for England.
Published in the Archives of Pediatrics & Adolescent Medicine, the study found that there is a strong association between children's and parents' body size.
When both parents were in the thinner half of the healthy weight range, the chance of the child being thin was 16.2 per cent, compared with 7.8 per cent when both parents were in the upper half of range.
In comparison, 5.3 per cent of children with two overweight parents are likely to be thin.
Lead author Dr Katriina Whitaker, UCL epidemiology and public health specialist, commented: "We know from other studies that children's weights are correlated with those of their parents, but previous research has tended to focus on obesity rather than the other end of the spectrum."
A further study published in Obesity suggested that green tea could decrease the risk of obesity after lab tests on mice showed positive results...
Thinner children are therefore more likely to come from slimmer families, researchers at University College London (UCL) have found through a national health survey for England.
Published in the Archives of Pediatrics & Adolescent Medicine, the study found that there is a strong association between children's and parents' body size.
When both parents were in the thinner half of the healthy weight range, the chance of the child being thin was 16.2 per cent, compared with 7.8 per cent when both parents were in the upper half of range.
In comparison, 5.3 per cent of children with two overweight parents are likely to be thin.
Lead author Dr Katriina Whitaker, UCL epidemiology and public health specialist, commented: "We know from other studies that children's weights are correlated with those of their parents, but previous research has tended to focus on obesity rather than the other end of the spectrum."
A further study published in Obesity suggested that green tea could decrease the risk of obesity after lab tests on mice showed positive results...
Carbs may suppress fat absorption and accumulation: Animal data
Dietary fructooligosaccharides – carbohydrates with established prebiotic activity – may suppress high-fat diet-induced body fat accumulation, and inhibit intestinal absorption of dietary fats, say researchers.
Writing in the journal BioFactors, researchers investigated the effects of fructooligosaccharides (FOS) on the development of obesity, using two experiments in rats and mice. They found that body weight and percent body fat were lower in mice fed FOS than in controls, whilst rats receiving an oral dose of FOS were reported to have suppressed elevation of plasma triglycerides.
“We have shown that a low dose of dietary FOS suppressed weight gain, accumulation of visceral adipose [fat] tissue, and the increase in liver triglycerides resulting from feeding a high-fat ‘western’ diet ... while fat excretion increased,” reported the authors, led by Yuko Nakamura from the Food and Health R&D Laboratories at the Japanese pharmaceutical company Meiji Seika Kaisha.
“These results suggest that FOS may prevent fat accumulation by inhibiting intestinal absorption of dietary fat in a high-fat ‘western’ diet,” added the researchers...
Writing in the journal BioFactors, researchers investigated the effects of fructooligosaccharides (FOS) on the development of obesity, using two experiments in rats and mice. They found that body weight and percent body fat were lower in mice fed FOS than in controls, whilst rats receiving an oral dose of FOS were reported to have suppressed elevation of plasma triglycerides.
“We have shown that a low dose of dietary FOS suppressed weight gain, accumulation of visceral adipose [fat] tissue, and the increase in liver triglycerides resulting from feeding a high-fat ‘western’ diet ... while fat excretion increased,” reported the authors, led by Yuko Nakamura from the Food and Health R&D Laboratories at the Japanese pharmaceutical company Meiji Seika Kaisha.
“These results suggest that FOS may prevent fat accumulation by inhibiting intestinal absorption of dietary fat in a high-fat ‘western’ diet,” added the researchers...
Discover Key Protein Responsible for Fat Storage
UC Davis Health System researchers have discovered that a protein called galectin-12 plays a key role in fat storage, a finding that could lead to improvements in treating obesity and diabetes. The researchers found that without the ability to make the protein, mice used in their research investigation stored 40 percent less body fat and had increased fat metabolism and decreased insulin resistance.
"This study for the first time demonstrates the importance of a galectin in energy metabolism," said Fu-Tong Liu, distinguished professor and chair of the UC Davis Department of Dermatology, and senior author on the paper.
The findings, published online this week in the early edition of the Proceedings of the National Academy of Sciences, point to galectin-12 as a potential target for the treatment of obesity and diabetes in humans. The breakdown and storage of fat in the body are both tightly controlled processes that involve numerous chemical signals, Liu said.
"In this case, galectin-12 seems to be signaling to fat cells that its time to conserve rather than burn energy," he said. "If we can interrupt that signal, we have a chance at improving fat metabolism and reducing insulin resistance in patients with obesity and type 2 diabetes."
Obesity is the number-one predictor for the development of diabetes, a leading cause of death and disability in the United States. An estimated 24 million Americans have the disease. Between 90 and 95 percent of them have type 2 diabetes, and about 80 percent of people with type 2 diabetes are overweight or obese.
In its early stages, type 2 diabetes is characterized by insulin resistance. The pancreas is producing insulin, but for unknown reasons the body cannot use the insulin effectively. After several years, insulin production decreases, glucose builds up in the blood and the body cannot make efficient use of its main source of fuel. People with advanced diabetes may experience blindness, require limb amputations or suffer fatal organ failure.
In order to discover potential treatments for type 2 diabetes, Liu and his UC Davis colleagues have been working to understand the chemical signals involved in normal energy metabolism and storage. They isolated and cloned the galectin-12 gene 10 years ago. Since then, their studies have shown that the gene is preferentially expressed in fat cells, and that its expression is required for fat-cell differentiation. To enable a focus on specific biological mechanisms associated with galectin-12, the researchers worked with the UC Davis Mouse Biology Program to obtain genetically customized mice that have had individual genes systematically turned off or "knocked out."
"We decided to create the galectin-12 knockout mice to further clarify the function of this protein in animals," said Ri-Yao Yang, associate project scientist...
"This study for the first time demonstrates the importance of a galectin in energy metabolism," said Fu-Tong Liu, distinguished professor and chair of the UC Davis Department of Dermatology, and senior author on the paper.
The findings, published online this week in the early edition of the Proceedings of the National Academy of Sciences, point to galectin-12 as a potential target for the treatment of obesity and diabetes in humans. The breakdown and storage of fat in the body are both tightly controlled processes that involve numerous chemical signals, Liu said.
"In this case, galectin-12 seems to be signaling to fat cells that its time to conserve rather than burn energy," he said. "If we can interrupt that signal, we have a chance at improving fat metabolism and reducing insulin resistance in patients with obesity and type 2 diabetes."
Obesity is the number-one predictor for the development of diabetes, a leading cause of death and disability in the United States. An estimated 24 million Americans have the disease. Between 90 and 95 percent of them have type 2 diabetes, and about 80 percent of people with type 2 diabetes are overweight or obese.
In its early stages, type 2 diabetes is characterized by insulin resistance. The pancreas is producing insulin, but for unknown reasons the body cannot use the insulin effectively. After several years, insulin production decreases, glucose builds up in the blood and the body cannot make efficient use of its main source of fuel. People with advanced diabetes may experience blindness, require limb amputations or suffer fatal organ failure.
In order to discover potential treatments for type 2 diabetes, Liu and his UC Davis colleagues have been working to understand the chemical signals involved in normal energy metabolism and storage. They isolated and cloned the galectin-12 gene 10 years ago. Since then, their studies have shown that the gene is preferentially expressed in fat cells, and that its expression is required for fat-cell differentiation. To enable a focus on specific biological mechanisms associated with galectin-12, the researchers worked with the UC Davis Mouse Biology Program to obtain genetically customized mice that have had individual genes systematically turned off or "knocked out."
"We decided to create the galectin-12 knockout mice to further clarify the function of this protein in animals," said Ri-Yao Yang, associate project scientist...
Gene clue to diabetes sufferers
Scientists have identified a gene that could explain why some people are more susceptible than others to diabetes.
The gene, found in tests on obese mice, controls a protein called tomosyn-2 which acts as a brake on insulin secretion from the pancreas, the researchers also discovered.
Insulin is made and released by beta cells in the pancreas and regulates blood sugars. Those with type 1 diabetes have too little insulin, while those with type 2 are insulin-resistant - both conditions potentially causing serious health problems if they are not treated.
Alan Attie, of the University of Wisconsin-Madison, who led the study, said: "It's too early for us to know how relevant this gene will be to human diabetes, but the concept of negative regulation is one of the most interesting things to come out of this study and that very likely applies to humans."
The researchers studied obese mice as it takes more insulin to lower glucose for an obese person than someone of a healthy weight...
The gene, found in tests on obese mice, controls a protein called tomosyn-2 which acts as a brake on insulin secretion from the pancreas, the researchers also discovered.
Insulin is made and released by beta cells in the pancreas and regulates blood sugars. Those with type 1 diabetes have too little insulin, while those with type 2 are insulin-resistant - both conditions potentially causing serious health problems if they are not treated.
Alan Attie, of the University of Wisconsin-Madison, who led the study, said: "It's too early for us to know how relevant this gene will be to human diabetes, but the concept of negative regulation is one of the most interesting things to come out of this study and that very likely applies to humans."
The researchers studied obese mice as it takes more insulin to lower glucose for an obese person than someone of a healthy weight...
Green Tea May Help You Lose Weight
Drinking green tea can slow down weight gain by limiting the amount of fat absorbed by the body, the Daily Mail reported Wednesday.
In a new study, Penn State University researchers found that a compound in the herbal tea slowed down weight gain in mice.
Crucially, the mice were already obese at the start of the experiment. This makes the findings more relevant to humans because people often consider dietary changes only when they notice problems associated with obesity, the researchers said...
In a new study, Penn State University researchers found that a compound in the herbal tea slowed down weight gain in mice.
Crucially, the mice were already obese at the start of the experiment. This makes the findings more relevant to humans because people often consider dietary changes only when they notice problems associated with obesity, the researchers said...
Scientists identify genes involved in storing fat
Researchers funded by the Wellcome Trust have identified several genes in fat tissue that may lead us to retain fat unnecessarily in the body. The study, using a mouse model, may explain why some people carry more weight than others even when they have similar diets because of genes that encourage fat storage.
Scientists at the University of Edinburgh compared fat tissue from mice that had been selectively bred for many generations to be increasingly fat or thin, and as a result had acquired weight-related genes. The research, published in the journal ’PLoS One’, cross-referenced thousands of genes and pinpointed genes that prevented the breakdown of fat, which were more prevalent in the fat tissue of the overweight mice than in the fat tissue of the lean mice.
Mice were then bred from one overweight parent and one lean parent. Those among the offspring that were born overweight were found to have the same active genes as the fatter parent mice - an indication that hereditary factors play a part in fat storage and can increase the likelihood of putting on weight.
The research also found that the thin offspring had an added protection against weight gain. When both sets of mice were given fatty foods, the thin offspring seemed able to break down fatty tissue more easily than the heavier mice, suggesting they had inherited ’lean genes’...
Scientists at the University of Edinburgh compared fat tissue from mice that had been selectively bred for many generations to be increasingly fat or thin, and as a result had acquired weight-related genes. The research, published in the journal ’PLoS One’, cross-referenced thousands of genes and pinpointed genes that prevented the breakdown of fat, which were more prevalent in the fat tissue of the overweight mice than in the fat tissue of the lean mice.
Mice were then bred from one overweight parent and one lean parent. Those among the offspring that were born overweight were found to have the same active genes as the fatter parent mice - an indication that hereditary factors play a part in fat storage and can increase the likelihood of putting on weight.
The research also found that the thin offspring had an added protection against weight gain. When both sets of mice were given fatty foods, the thin offspring seemed able to break down fatty tissue more easily than the heavier mice, suggesting they had inherited ’lean genes’...
Fat content in mice affected by environment
A recent study found that mice living in socially enriching environments converted a greater portion of their energy-storing white fat to energy-burning brown fat, losing weight despite their increased caloric intake. These findings reinforce how social and physical environments can impact animal metabolisms.
Adipose tissue, commonly known as fat, comes in two types: white and brown. White fat, which constitutes as much as 20 percent of the body weight in men and 25 percent of the body weight in women, serves to store excess energy, cushion organs and maintain body temperature. Brown fat, which is especially abundant in newborns and hibernating mammals, expends energy to generate heat. Increases in white fat and brown fat concentrations are associated with weight gain and loss, respectively.
Functional differences between white and brown fat are predicted by differences in structure. White adipocytes contain a single, large lipid droplet that occupies most of the cell volume. In contrast, brown adipocytes contain numerous small droplets, more iron-containing mitochondria, which explains the characteristic brown color, and more capillaries to deliver greater amounts of oxygen.
While brown fat is best known for its role in insulating infants, scientists found that active brown fat is also present in adults. In addition, cold exposure and activation of the sympathetic nervous system drives the production of more brown fat. The new study, whose results are published in the September issue of Cell Metabolism, suggests that an engaging environment can provide another, perhaps more effective means to increase brown fat.
According to Lei Cao of The Ohio State University, the typical laboratory mouse leads what might be considered a "couch potato" lifestyle. Lab mice are given free access to food and water, as well as a few potential playmates. However, they are not given much else to do.
In the enriched environment, mice live in groups of 15 to 20. They are given more space as well as exercise wheels, mazes and toys. After four weeks in the enriched environment, the mice's abdominal fat decreased by 50 percent...
Adipose tissue, commonly known as fat, comes in two types: white and brown. White fat, which constitutes as much as 20 percent of the body weight in men and 25 percent of the body weight in women, serves to store excess energy, cushion organs and maintain body temperature. Brown fat, which is especially abundant in newborns and hibernating mammals, expends energy to generate heat. Increases in white fat and brown fat concentrations are associated with weight gain and loss, respectively.
Functional differences between white and brown fat are predicted by differences in structure. White adipocytes contain a single, large lipid droplet that occupies most of the cell volume. In contrast, brown adipocytes contain numerous small droplets, more iron-containing mitochondria, which explains the characteristic brown color, and more capillaries to deliver greater amounts of oxygen.
While brown fat is best known for its role in insulating infants, scientists found that active brown fat is also present in adults. In addition, cold exposure and activation of the sympathetic nervous system drives the production of more brown fat. The new study, whose results are published in the September issue of Cell Metabolism, suggests that an engaging environment can provide another, perhaps more effective means to increase brown fat.
According to Lei Cao of The Ohio State University, the typical laboratory mouse leads what might be considered a "couch potato" lifestyle. Lab mice are given free access to food and water, as well as a few potential playmates. However, they are not given much else to do.
In the enriched environment, mice live in groups of 15 to 20. They are given more space as well as exercise wheels, mazes and toys. After four weeks in the enriched environment, the mice's abdominal fat decreased by 50 percent...
Tuesday, August 30, 2011
Black tea extract prevents obesity
There are many diets you can try to avoid or prevent obesity. But chances are good that none of them work for you. The problem is that most people couldn't control their daily intake of calories because foods with high fat, high salt and high sugar taste just too good.
New research suggests that simply taking some extract of a Chinese black tea called Pu-Erh tea after meals may help you stop gaining weight even if you continue eating a typical obesity-inducing Western diet full of high fat, high protein and high energy.
The research conducted by Yasuyuki Oi of Nippon Supplement, Inc. based out of Osaka, Japan found mice given the black tea extract in some dose did not raise levels of blood triglycerides after ingestion of a corn oil emulsion.
The researchers published the results in Phytotherapy Research. In the research, female ddy mice were given one of seven diets with either high fat, or a normal dietary composition, or supplemented black tea extract, or gallic acid in different doses for a period of 12 weeks...
New research suggests that simply taking some extract of a Chinese black tea called Pu-Erh tea after meals may help you stop gaining weight even if you continue eating a typical obesity-inducing Western diet full of high fat, high protein and high energy.
The research conducted by Yasuyuki Oi of Nippon Supplement, Inc. based out of Osaka, Japan found mice given the black tea extract in some dose did not raise levels of blood triglycerides after ingestion of a corn oil emulsion.
The researchers published the results in Phytotherapy Research. In the research, female ddy mice were given one of seven diets with either high fat, or a normal dietary composition, or supplemented black tea extract, or gallic acid in different doses for a period of 12 weeks...
Will new wonder drug let humans 'have their cake and eat it, too?'
Imagine a drug that combines an ingredient found in red wine, which extends your life on the provision you eat as much as you please, eventually becoming obese. Sound too good to be true? Those are the provisions of the new drug called SRT-1720, and the success found in obese lab mice has been amazing.
LOS ANGELES, CA (Catholic Online) - SRT-1720 is an experimental agent, which in different forms is also being tested in humans. The drug found to prevent some of the life-shortening diseases associated with obesity in mice, by curbing levels of fat in the liver and improving sensitivity to insulin.
SRT-1720 is based on the compound resveratrol, which is found in red wine and is thought to combat some of the effects of aging by boosting levels of proteins called sirtuins. These are the proteins that have been associated with 30 percent life extension in mice and rats put on low-calorie diets.
Developed by David Sinclair, a biologist at Harvard Medical School and one of the co-authors of the current mouse study, the findings associated with SRT-1720 appear in the new journal Scientific Reports...
LOS ANGELES, CA (Catholic Online) - SRT-1720 is an experimental agent, which in different forms is also being tested in humans. The drug found to prevent some of the life-shortening diseases associated with obesity in mice, by curbing levels of fat in the liver and improving sensitivity to insulin.
SRT-1720 is based on the compound resveratrol, which is found in red wine and is thought to combat some of the effects of aging by boosting levels of proteins called sirtuins. These are the proteins that have been associated with 30 percent life extension in mice and rats put on low-calorie diets.
Developed by David Sinclair, a biologist at Harvard Medical School and one of the co-authors of the current mouse study, the findings associated with SRT-1720 appear in the new journal Scientific Reports...
Slim down by targeting the hormone uroguanylin
The number of people who are obese and suffer one or more of its associated health problems (including type 2 diabetes) is escalating dramatically. Researchers are seeking to identify new targets for therapeutics that could limit appetite and thereby obesity. A team of researchers, led by Scott Waldman, at Thomas Jefferson University, Philadelphia, has now uncovered one such potential target by studying the molecular control of appetite in mice.
In the study, Waldman and colleagues found that nutrient intake by mice caused cells in their gut to secrete the precursor of the hormone uroguanylin (prouroguanylin) into the blood...
In the study, Waldman and colleagues found that nutrient intake by mice caused cells in their gut to secrete the precursor of the hormone uroguanylin (prouroguanylin) into the blood...
Genetics' new frontier: What mom eats, weighs in pregnancy can set child up for obesity, diabetes
Cracking the human genome is already old news for those riding the next wave of genetic research. The rising field of epigenetics is revealing how diet, behavior and the environment are reprogramming the genes we're dealt at conception.
Although your DNA was locked in the moment your parents' egg and sperm met, how those genes get expressed depends on what happened next. "Most chronic diseases that occur in adulthood have their origins in the first 1,000 days after conception," said Kent Thornburg, an epigenetics researcher at Oregon Health and Science University.
What's more, the epigenetic changes that happen in the womb get passed on to future generations.
Sorry, moms. That means once again, the pressure is on you.
"If your mom was obese while she was pregnant with you, you're marked," said Philip Wood, professor at Sanford Burnham Research Institute in Lake Nona. You will have an uphill battle fighting off excess weight and its ill effects, including diabetes and heart disease, even if you're adopted and raised by slim parents, he said.
The findings are significant as medical science works to identify causes and cures for the two most serious and costly epidemics facing America: obesity and diabetes.
We don't understand all of the mechanisms, but they likely involve maternal circulating hormones, such as leptin and insulin, and glucose levels that can alter how the placenta develops and what nutrients cross it, said Tracy Bale, associate professor of neuroscience at the University of Pennsylvania School of Veterinary Medicine, who has done epigenetic studies on animals.
Studies have shown that these effects can be handed down to the next generation, she added.
Rewriting the script
Epigenetics can silence or draw out the expression of genes.
"If DNA is the hardware, epigenetics is the software that tells genes what to do," said Randy Jirtle, an epigenetics researcher at Duke University Medical Center.
A study conducted on mice, and published in 2003 in Molecular Cell Biology, illustrated the effects of diet on genes. The mice in the study carried the agouti gene, which humans also have.
When scientists fed pregnant mice a certain diet that silenced the gene, the baby mice came out yellow, fat and prone to diabetes and cancer. When they fed the mice diets that activated the gene — a diet rich in folic acid, B vitamins and choline — mice came out skinny, brown and not susceptible to disease.
"The mice were genetically identical," said Jirtle, who was part of the study. "The only difference was what the mothers ate."
Granted these are mice, not humans, he added, "but the experiment showed that a mother's diet can shape the epigenome of her offspring."...
Although your DNA was locked in the moment your parents' egg and sperm met, how those genes get expressed depends on what happened next. "Most chronic diseases that occur in adulthood have their origins in the first 1,000 days after conception," said Kent Thornburg, an epigenetics researcher at Oregon Health and Science University.
What's more, the epigenetic changes that happen in the womb get passed on to future generations.
Sorry, moms. That means once again, the pressure is on you.
"If your mom was obese while she was pregnant with you, you're marked," said Philip Wood, professor at Sanford Burnham Research Institute in Lake Nona. You will have an uphill battle fighting off excess weight and its ill effects, including diabetes and heart disease, even if you're adopted and raised by slim parents, he said.
The findings are significant as medical science works to identify causes and cures for the two most serious and costly epidemics facing America: obesity and diabetes.
We don't understand all of the mechanisms, but they likely involve maternal circulating hormones, such as leptin and insulin, and glucose levels that can alter how the placenta develops and what nutrients cross it, said Tracy Bale, associate professor of neuroscience at the University of Pennsylvania School of Veterinary Medicine, who has done epigenetic studies on animals.
Studies have shown that these effects can be handed down to the next generation, she added.
Rewriting the script
Epigenetics can silence or draw out the expression of genes.
"If DNA is the hardware, epigenetics is the software that tells genes what to do," said Randy Jirtle, an epigenetics researcher at Duke University Medical Center.
A study conducted on mice, and published in 2003 in Molecular Cell Biology, illustrated the effects of diet on genes. The mice in the study carried the agouti gene, which humans also have.
When scientists fed pregnant mice a certain diet that silenced the gene, the baby mice came out yellow, fat and prone to diabetes and cancer. When they fed the mice diets that activated the gene — a diet rich in folic acid, B vitamins and choline — mice came out skinny, brown and not susceptible to disease.
"The mice were genetically identical," said Jirtle, who was part of the study. "The only difference was what the mothers ate."
Granted these are mice, not humans, he added, "but the experiment showed that a mother's diet can shape the epigenome of her offspring."...
Saturday, August 27, 2011
How fatty food triggers diabetes: Scientists believe discovery paves way for Type 2 'cure'
Fatty food trips a genetic switch in the body that can trigger diabetes, a study has found.
Understanding the biological pathway could lead to a potential cure for the disease, say scientists.
The discovery helps explain why Type 2 diabetes is so often linked to obesity.
In studies of mice and humans, researchers found that high levels of fat disrupted two key proteins that turn genes on and off...
Understanding the biological pathway could lead to a potential cure for the disease, say scientists.
The discovery helps explain why Type 2 diabetes is so often linked to obesity.
In studies of mice and humans, researchers found that high levels of fat disrupted two key proteins that turn genes on and off...
Fat Mice Live Longer With Novel Drug
An investigational compound extended survival in middle-age, obese male mice that were eating a high-fat diet, but researchers warned that it was too soon to say if the drug could do the same for humans.
Three groups of mice all gained a similar amount of weight during the study, but those that ate a low dose of SRT1720 lived 4% longer and those that ate a high dose lived 18% longer than their untreated counterparts (P<0.001), Rafael de Cabo, PhD, of the National Institute on Aging's Laboratory of Experimental Gerontology in Baltimore, and colleagues, wrote online in Scientific Reports...
Three groups of mice all gained a similar amount of weight during the study, but those that ate a low dose of SRT1720 lived 4% longer and those that ate a high dose lived 18% longer than their untreated counterparts (P<0.001), Rafael de Cabo, PhD, of the National Institute on Aging's Laboratory of Experimental Gerontology in Baltimore, and colleagues, wrote online in Scientific Reports...
Saturday, August 20, 2011
Compound improves health, increases lifespan of obese mice
Researchers have reported that obese male mice treated with a synthetic compound called SRT1720 were healthier and lived longer compared to non-treated obese mice. The experimental compound was found to improve the function of the liver, pancreas and heart in mice.
The National Institute on Aging (NIA) supported the study, in collaboration with Sirtris, a GlaxoSmithKline company. The study was primarily conducted by the NIA, part of the National Institutes of Health, and is published online in the Thursday, August 18, 2011, issue of Scientific Reports.
"This study has interesting implications for research on the biology of aging. It demonstrates that years of healthy life can be extended in an animal model of diet-induced obesity by a synthetic compound that modulates a gene pathway associated with aging," said NIA Director Richard J. Hodes, M.D. More research is needed to assess the relevance of these findings in people, Hodes and the researchers noted.
SRT1720, a patented molecule, has been shown to activate the SIRT1enzyme, part of a class of enzymes called sirtuins. Sirtuins have been previously implicated in aging processes and are thought to contribute to the positive effects of dietary restriction (also known as calorie restriction) in higher organisms, including nonhuman primates.
In this study, scientists compared the health of 1-year-old, or middle-aged, male mice fed a high-fat diet with a high dose of SRT1720, a low dose of SRT1720 or no SRT1720. Additionally, these mice were compared to a control group of 1-year-old male mice fed a standard diet...
The National Institute on Aging (NIA) supported the study, in collaboration with Sirtris, a GlaxoSmithKline company. The study was primarily conducted by the NIA, part of the National Institutes of Health, and is published online in the Thursday, August 18, 2011, issue of Scientific Reports.
"This study has interesting implications for research on the biology of aging. It demonstrates that years of healthy life can be extended in an animal model of diet-induced obesity by a synthetic compound that modulates a gene pathway associated with aging," said NIA Director Richard J. Hodes, M.D. More research is needed to assess the relevance of these findings in people, Hodes and the researchers noted.
SRT1720, a patented molecule, has been shown to activate the SIRT1enzyme, part of a class of enzymes called sirtuins. Sirtuins have been previously implicated in aging processes and are thought to contribute to the positive effects of dietary restriction (also known as calorie restriction) in higher organisms, including nonhuman primates.
In this study, scientists compared the health of 1-year-old, or middle-aged, male mice fed a high-fat diet with a high dose of SRT1720, a low dose of SRT1720 or no SRT1720. Additionally, these mice were compared to a control group of 1-year-old male mice fed a standard diet...
Sunday, August 14, 2011
Brown Fat, Also Known As Good Fat, More Common In Leaner Children
Investigators at Joslin Diabetes Center and Children's Hospital Boston have revealed that a type of "good" fat known as brown fat occurs in varying amounts in children which increases until puberty and then declines. Brown fat is more common in children who are leaner...
In 2010 a Joslin investigation identified cells in mice that can be triggered to transform into brown fat....
In 2010 a Joslin investigation identified cells in mice that can be triggered to transform into brown fat....
Brain Protein ‘Nesfatin-1’ Shows Promise In Checking Obesity
Study conducted by an Indian-origin researcher showed that protein present in human brain may actually hold the key to keeping hunger and blood glucose in hand and keep unwanted pounds away.
Associate professor in biology at Canada's York University, Suraj Unniappan is investigating the metabolic effects of a protein known as nesfatin-1 present within the human brain.
Prof Suraj discovered that rats fed nesfatin-1 consumed less, utilized extra stored fat and turned more active.
In addition, it induced insulin discharge from the pancreatic beta cells of both rats and mice...
Associate professor in biology at Canada's York University, Suraj Unniappan is investigating the metabolic effects of a protein known as nesfatin-1 present within the human brain.
Prof Suraj discovered that rats fed nesfatin-1 consumed less, utilized extra stored fat and turned more active.
In addition, it induced insulin discharge from the pancreatic beta cells of both rats and mice...
York U Researchers Zero In On Protein That May Help Treat Obesity, Diabetes
A newly-identified protein may hold the key to keeping appetite and blood sugar in check, according to a study by York University researchers.
Suraj Unniappan, associate professor in York's Department of Biology, Faculty of Science & Engineering, is delving into the metabolic effects of a protein called nesfatin-1, abundantly present in the brain. His studies found that rats administered with nesfatin-1 ate less, used more stored fat and became more active. In addition, the protein stimulated insulin secretion from the pancreatic beta cells of both rats and mice.
"[The rats] actually ate more frequently but in lesser amounts," says Unniappan, a member of York's neuroscience graduate diploma program, and a recipient of a Canadian Institutes of Health Research (CIHR) New Investigator Award. "In addition, they were more active and we found that their fatty acid oxidization was increased. In other words, the energy reserve being preferably used during nesfatin-1 treatment was fat. This suggests more fat loss, which could eventually result in body weight loss," he says....
Suraj Unniappan, associate professor in York's Department of Biology, Faculty of Science & Engineering, is delving into the metabolic effects of a protein called nesfatin-1, abundantly present in the brain. His studies found that rats administered with nesfatin-1 ate less, used more stored fat and became more active. In addition, the protein stimulated insulin secretion from the pancreatic beta cells of both rats and mice.
"[The rats] actually ate more frequently but in lesser amounts," says Unniappan, a member of York's neuroscience graduate diploma program, and a recipient of a Canadian Institutes of Health Research (CIHR) New Investigator Award. "In addition, they were more active and we found that their fatty acid oxidization was increased. In other words, the energy reserve being preferably used during nesfatin-1 treatment was fat. This suggests more fat loss, which could eventually result in body weight loss," he says....
Medical: In the obesity battle, it's mind over stomach
...Last winter, Baylor College of Medicine scientists reported working with mice genetically modified to lack a receptor for the ghrelin hormone.
They found this turned up the fat-burning thermostat in the animals' bodies. In an older group of the mice, the rodents were slimmer than a control group even though they ate just as much and were no more physically active.
Still another mouse study, reported in this month's Cell Metabolism, looked more closely at what happens inside the hypothalamus and found that when they are starved, some neurons in that part of the brain actually start eating bits of themselves, which in turn ramps up hormonal signals to start eating.
Such cellular cannibalism goes on all the time as part of the body's natural housekeeping, but the discovery that this process also helps regulate appetite opens a new possible route for obesity-fighting drugs....
They found this turned up the fat-burning thermostat in the animals' bodies. In an older group of the mice, the rodents were slimmer than a control group even though they ate just as much and were no more physically active.
Still another mouse study, reported in this month's Cell Metabolism, looked more closely at what happens inside the hypothalamus and found that when they are starved, some neurons in that part of the brain actually start eating bits of themselves, which in turn ramps up hormonal signals to start eating.
Such cellular cannibalism goes on all the time as part of the body's natural housekeeping, but the discovery that this process also helps regulate appetite opens a new possible route for obesity-fighting drugs....
Wednesday, August 10, 2011
A Protein May Help Treat Obesity, Diabetes
A newly-identified protein may hold the key to keeping appetite and blood sugar in check, according to a study by York University researchers.
Suraj Unniappan, associate professor in York's Department of Biology, Faculty of Science & Engineering, is delving into the metabolic effects of a protein called nesfatin-1, abundantly present in the brain. His studies found that rats administered with nesfatin-1 ate less, used more stored fat and became more active. In addition, the protein stimulated insulin secretion from the pancreatic beta cells of both rats and mice.
"[The rats] actually ate more frequently but in lesser amounts," says Unniappan, a member of York's neuroscience graduate diploma program, and a recipient of a Canadian Institutes of Health Research (CIHR) New Investigator Award. "In addition, they were more active and we found that their fatty acid oxidization was increased. In other words, the energy reserve being preferably used during nesfatin-1 treatment was fat. This suggests more fat loss, which could eventually result in body weight loss," he says.
The findings were reported in two recent research articles from Unniappan's laboratory: one published August 9 in Endocrinology and another in March 2011 in Journal of Endocrinology.
Discovered by a research team from Japan in 2006, nesfatin-1 was earlier found to regulate appetite and the production of body fat when injected into the brain of mice and rats...
Suraj Unniappan, associate professor in York's Department of Biology, Faculty of Science & Engineering, is delving into the metabolic effects of a protein called nesfatin-1, abundantly present in the brain. His studies found that rats administered with nesfatin-1 ate less, used more stored fat and became more active. In addition, the protein stimulated insulin secretion from the pancreatic beta cells of both rats and mice.
"[The rats] actually ate more frequently but in lesser amounts," says Unniappan, a member of York's neuroscience graduate diploma program, and a recipient of a Canadian Institutes of Health Research (CIHR) New Investigator Award. "In addition, they were more active and we found that their fatty acid oxidization was increased. In other words, the energy reserve being preferably used during nesfatin-1 treatment was fat. This suggests more fat loss, which could eventually result in body weight loss," he says.
The findings were reported in two recent research articles from Unniappan's laboratory: one published August 9 in Endocrinology and another in March 2011 in Journal of Endocrinology.
Discovered by a research team from Japan in 2006, nesfatin-1 was earlier found to regulate appetite and the production of body fat when injected into the brain of mice and rats...
Sunday, August 07, 2011
Mimicking Calorie Restriction to Fight Obesity and Type 2 Diabetes
A Yale University-led research team has discovered how reduced expression of a particular gene protects against obesity and type 2 diabetes, possibly prolonging lifespan by mimicking the effects of calorie restriction. The study appears in the August 3 issue of Cell Metabolism.
It is known that excess calorie consumption leads to obesity, insulin resistance and increased mortality, whereas calorie restriction reduces accumulation of body fat and improves cellular energy balance and insulin action – reversing obesity and type 2 diabetes, delaying the aging process, and prolonging life in primates and many other species.
It has also been shown in the past that reduced expression of the so-called “INDY” gene in D. Melanogaster flies and C. elegans worms promotes longevity in a manner similar to calorie restriction. But until now, the cellular mechanism by which this happens was unknown.
The Yale team generated a mouse with the so-called “INDY” gene deleted. Loss of the gene altered chemical levels in the cellular signaling network in a way that improved mitochondrial action in the liver, metabolism of fatty acids, and cellular energy transport. Overall, these traits protected the mice from diet-related accumulation of body fat and insulin resistance that evolve, as we age, into type 2 diabetes...
It is known that excess calorie consumption leads to obesity, insulin resistance and increased mortality, whereas calorie restriction reduces accumulation of body fat and improves cellular energy balance and insulin action – reversing obesity and type 2 diabetes, delaying the aging process, and prolonging life in primates and many other species.
It has also been shown in the past that reduced expression of the so-called “INDY” gene in D. Melanogaster flies and C. elegans worms promotes longevity in a manner similar to calorie restriction. But until now, the cellular mechanism by which this happens was unknown.
The Yale team generated a mouse with the so-called “INDY” gene deleted. Loss of the gene altered chemical levels in the cellular signaling network in a way that improved mitochondrial action in the liver, metabolism of fatty acids, and cellular energy transport. Overall, these traits protected the mice from diet-related accumulation of body fat and insulin resistance that evolve, as we age, into type 2 diabetes...
Obesity ups risk of diabetes
Scientists at Joslin Diabetes Center have found how obesity drives insulin resistance, the condition that may lead to type 2 diabetes.
They uncovered that excess weight wreaks its havoc by altering the production of proteins that affect how other proteins are spliced together.
The finding may point toward novel targets for diabetes drugs.
Scientists in the lab of Mary-Elizabeth Patti, M.D., began by examining the levels of proteins in the livers of obese people, and finding decreases in number for certain proteins that regulate RNA splicing.
"When a gene is transcribed by the cell, it generates a piece of RNA," stated Dr. Patti, who is also an Assistant Professor of Medicine at Harvard Medical School.
"That piece of RNA can be split up in different ways, generating proteins that have different functions.
"In the case of these proteins whose production drops in the livers of obese people, this process changes the function of other proteins that can cause excess fat to be made in the liver.
"That excess fat is known to be a major contributor to insulin resistance," she explained.
The investigators went on to examine a representative RNA-splicing protein called SFRS10 whose levels drop in muscle and liver both in obese people and in over-fed mice...
They uncovered that excess weight wreaks its havoc by altering the production of proteins that affect how other proteins are spliced together.
The finding may point toward novel targets for diabetes drugs.
Scientists in the lab of Mary-Elizabeth Patti, M.D., began by examining the levels of proteins in the livers of obese people, and finding decreases in number for certain proteins that regulate RNA splicing.
"When a gene is transcribed by the cell, it generates a piece of RNA," stated Dr. Patti, who is also an Assistant Professor of Medicine at Harvard Medical School.
"That piece of RNA can be split up in different ways, generating proteins that have different functions.
"In the case of these proteins whose production drops in the livers of obese people, this process changes the function of other proteins that can cause excess fat to be made in the liver.
"That excess fat is known to be a major contributor to insulin resistance," she explained.
The investigators went on to examine a representative RNA-splicing protein called SFRS10 whose levels drop in muscle and liver both in obese people and in over-fed mice...
Dieting Leads to Self-Cannibalization of the Brain: Study
Dieting makes brain cells eat themselves, researchers said Wednesday.
In a new report, scientists say that hunger-inducing neurons consume themselves for energy during periods of starvation. This causes the body to produce fatty acids, which increases the amount of AgRP in the brain. AgRP is a hunger-signaling peptide that raises the desire to eat.
The study was conducted on lab mice, and published in the journal Cell Metabolism. The metabolic processes between mice and humans are very similar, according to the Los Angeles Times, especially when it comes to feeling hungry...
In a new report, scientists say that hunger-inducing neurons consume themselves for energy during periods of starvation. This causes the body to produce fatty acids, which increases the amount of AgRP in the brain. AgRP is a hunger-signaling peptide that raises the desire to eat.
The study was conducted on lab mice, and published in the journal Cell Metabolism. The metabolic processes between mice and humans are very similar, according to the Los Angeles Times, especially when it comes to feeling hungry...
Saturday, July 23, 2011
Krill Oil Reduces Ill Effects of High-Fat Diet
...The study results showed that feeding a high-fat diet to mice compared to animals given a low-fat diet led to an elevation of endocannabinoids (EC), lipid messengers that can activate specific receptors, thereby influencing not only enzyme activities, but also appetite, energy balance, mood, memory, and pain perception. In doing so, the EC system contributes to visceral fat accumulation. Superba krill oil was able to counteract the high fat diet-induced changes in EC levels after eight weeks of treatment. In addition to reducing EC levels in several different tissues, administration of krill oil also exerted lowering effects on triglyceride, cholesterol and a marker of inflammation...
For A Sugary Way Out Of Obesity!
Sugarcane extract could be a pleasant tool in the fight against obesity, Australian researchers believe. The results of the La Trobe University experiments on mice and reported in Nutrition Horizon, may provide a new approach for weight management in humans.
The study was carried out by Dr Richard Weisinger with La Trobe colleagues Dr Lauren Stahl, Dr Denovan Begg, Dr Mark Jois and collaborators Dr Ankur Desai and Dr Jason Smythe from Horizon Science, a Melbourne based food biotechnology firm. Their work was discussed at a meeting of the Society for the Study of Ingestive Behavior held in Clearwater, Florida, USA.
Molasses usually end up as a waste-product of sugar refining. However, they are rich in polyphenols, says Dr Weisinger, chemicals found in plants known for their antioxidant properties.
Researchers supplemented the high-fat diet of a group of laboratory mice with molasses for 12 weeks. They found that these mice had lower body weight, reduced body fat and decreased blood levels of leptin – a hormone involved in energy regulation, appetite and metabolism – than the control group.
Further analyses, says Dr Weisinger, revealed that molasses supplements led to increased energy excretion, i.e, more calories were lost in faeces. They also found increased gene expression for several liver and fat cell biomarkers of energy metabolism...
The study was carried out by Dr Richard Weisinger with La Trobe colleagues Dr Lauren Stahl, Dr Denovan Begg, Dr Mark Jois and collaborators Dr Ankur Desai and Dr Jason Smythe from Horizon Science, a Melbourne based food biotechnology firm. Their work was discussed at a meeting of the Society for the Study of Ingestive Behavior held in Clearwater, Florida, USA.
Molasses usually end up as a waste-product of sugar refining. However, they are rich in polyphenols, says Dr Weisinger, chemicals found in plants known for their antioxidant properties.
Researchers supplemented the high-fat diet of a group of laboratory mice with molasses for 12 weeks. They found that these mice had lower body weight, reduced body fat and decreased blood levels of leptin – a hormone involved in energy regulation, appetite and metabolism – than the control group.
Further analyses, says Dr Weisinger, revealed that molasses supplements led to increased energy excretion, i.e, more calories were lost in faeces. They also found increased gene expression for several liver and fat cell biomarkers of energy metabolism...
Monday, July 04, 2011
Leucine Reverses Ill Effects of High-Fat Diet
Doubling the amount of the branched chained amino acid (BCAA) leucine in a high-fat diet reversed many of negative metabolic effects associated with metabolic syndrome and caused an improvement in glucose tolerance and insulin signaling in a recent mouse study (PLoS ONE. May 23;6(6): e21187. DOI:10.1371/journal.pone.0021187). This study demonstrates how a single, simple dietary factor—leucine—can modify insulin resistance by acting on multiple tissues and at multiple levels of metabolism.
American researchers placed mice on either a normal or high-fat diet; both groups had twice the normal amount of dietary leucine added to their drinking water. After eight weeks on a high-fat diet, mice developed obesity, fatty liver, inflammatory changes in adipose tissue and insulin resistance, as well as alterations in metabolomic profile of amino acid metabolites, glucose and cholesterol metabolites, and fatty acids in liver, muscle, fat and serum.
However, doubling dietary leucine reversed many of the metabolite abnormalities and caused a marked improvement in glucose tolerance and insulin signaling even though the mice still gained weight. Increased dietary leucine was also associated with a decrease in liver disease and a decrease in inflammation in adipose tissue.
These data indicate that modest changes in a single environmental/nutrient factor can modify multiple metabolic and signaling pathways and modify high-fat diet induced metabolic syndrome by acting at a systemic level on multiple tissues. These data also suggest that increasing dietary leucine may provide an adjunct in the management of obesity-related insulin resistance.
Last year, leucine was found to not help muscle recovery, but this current study may give the miconutrient new life in metabolic syndrome products as opposed to sports nutrition products.
American researchers placed mice on either a normal or high-fat diet; both groups had twice the normal amount of dietary leucine added to their drinking water. After eight weeks on a high-fat diet, mice developed obesity, fatty liver, inflammatory changes in adipose tissue and insulin resistance, as well as alterations in metabolomic profile of amino acid metabolites, glucose and cholesterol metabolites, and fatty acids in liver, muscle, fat and serum.
However, doubling dietary leucine reversed many of the metabolite abnormalities and caused a marked improvement in glucose tolerance and insulin signaling even though the mice still gained weight. Increased dietary leucine was also associated with a decrease in liver disease and a decrease in inflammation in adipose tissue.
These data indicate that modest changes in a single environmental/nutrient factor can modify multiple metabolic and signaling pathways and modify high-fat diet induced metabolic syndrome by acting at a systemic level on multiple tissues. These data also suggest that increasing dietary leucine may provide an adjunct in the management of obesity-related insulin resistance.
Last year, leucine was found to not help muscle recovery, but this current study may give the miconutrient new life in metabolic syndrome products as opposed to sports nutrition products.
Obese dieters' brain chemistry works against their weight-loss efforts
If you've been trying to lose weight and suspect your body's working against you, you may be right, according to a University of Illinois study published in Obesity.
"When obese persons reduce their food intake too drastically, their bodies appear to resist their weight loss efforts. They may have to work harder and go slower in order to outsmart their brain chemistry," said Gregory G. Freund, a professor in the U of I College of Medicine and a member of U of I's Division of Nutritional Sciences.
He particularly cautions against beginning a diet with a fast or cleansing day, which appears to trigger significant alterations in the immune system that work against weight loss. "Take smaller steps to start your weight loss and keep it going," he said.
In the study, the scientist compared the effects of a short-term fast on two groups of mice. For 12 weeks, one group consumed a low-fat diet (10 percent fat); the other group was fed a high-fat (60 percent fat) and had become obese. The mice were then fasted for 24 hours. In that time, the leaner mice lost 18 percent of their body weight compared to 5 percent for the obese mice.
Freund said that there is an immune component to weight loss that has not been recognized. "Our data show that fasting induces an anti-inflammatory effect on a lean animal's neuroimmune system, and that effect is inhibited by a high-fat diet. Some of the brain-based chemical changes that occur in a lean animal simply don't occur in an obese animal," he said.
This breakdown occurs because obese animals resist downregulation of genes that activate the interleukin-1 (IL-1) system and associated anti-inflammatory cytokines, he said.
The scientist also studied differences in the behavior of the two groups of mice, monitoring how much they moved, administering tests to discern the animals' ability to learn and remember, and noting whether the mice exhibited signs of depression or anxiety.
The results suggest that beginning a diet with a fast or near-fast may alter brain chemistry in a way that adversely affects mood and motivation, undermining the person's weight-loss efforts.
"The obese mice simply didn't move as much as the other mice. Not only was there reduced locomotion generally, they didn't burrow in the way that mice normally do, and that's associated with depression and anxiety," he said...
"When obese persons reduce their food intake too drastically, their bodies appear to resist their weight loss efforts. They may have to work harder and go slower in order to outsmart their brain chemistry," said Gregory G. Freund, a professor in the U of I College of Medicine and a member of U of I's Division of Nutritional Sciences.
He particularly cautions against beginning a diet with a fast or cleansing day, which appears to trigger significant alterations in the immune system that work against weight loss. "Take smaller steps to start your weight loss and keep it going," he said.
In the study, the scientist compared the effects of a short-term fast on two groups of mice. For 12 weeks, one group consumed a low-fat diet (10 percent fat); the other group was fed a high-fat (60 percent fat) and had become obese. The mice were then fasted for 24 hours. In that time, the leaner mice lost 18 percent of their body weight compared to 5 percent for the obese mice.
Freund said that there is an immune component to weight loss that has not been recognized. "Our data show that fasting induces an anti-inflammatory effect on a lean animal's neuroimmune system, and that effect is inhibited by a high-fat diet. Some of the brain-based chemical changes that occur in a lean animal simply don't occur in an obese animal," he said.
This breakdown occurs because obese animals resist downregulation of genes that activate the interleukin-1 (IL-1) system and associated anti-inflammatory cytokines, he said.
The scientist also studied differences in the behavior of the two groups of mice, monitoring how much they moved, administering tests to discern the animals' ability to learn and remember, and noting whether the mice exhibited signs of depression or anxiety.
The results suggest that beginning a diet with a fast or near-fast may alter brain chemistry in a way that adversely affects mood and motivation, undermining the person's weight-loss efforts.
"The obese mice simply didn't move as much as the other mice. Not only was there reduced locomotion generally, they didn't burrow in the way that mice normally do, and that's associated with depression and anxiety," he said...
Today's Oklahoma research may lead to skinny pills in tomorrow's pharmacy
Research that produced skinny mice conceivably could lead to tomorrow's skinny pill for humans, an Oklahoma Medical Research Foundation scientist says.
Scientist Lorin Olson added a mutant gene to laboratory mice with the expectation the cells would grow out of control and develop cancer. They didn't. But far more exciting was another thing the immature cells failed to do, he said. They did not turn into fat cells.
“Could this be real? What's really going on here?” Olson said he asked himself.
He watched those skinny mice closely.
“I saw that the mice weren't gaining weight and developing fat. But it could have been a lot of things,” he said...
Scientist Lorin Olson added a mutant gene to laboratory mice with the expectation the cells would grow out of control and develop cancer. They didn't. But far more exciting was another thing the immature cells failed to do, he said. They did not turn into fat cells.
“Could this be real? What's really going on here?” Olson said he asked himself.
He watched those skinny mice closely.
“I saw that the mice weren't gaining weight and developing fat. But it could have been a lot of things,” he said...
Wednesday, June 22, 2011
Anti-Obesity Vaccine Shows Positive Results
Researchers at the University of Porto in Portugal have developed a vaccine that fights obesity by suppressing the hormone ghrelin, which is an appetite stimulant.
“An anti-ghrelin vaccine may become an alternate treatment for obesity, to be used in combination with diet and exercise,” said lead investigator Dr. Mariana Monteiro. In other words, this vaccine may someday be a viable alternative to weight loss surgery.
The vaccine, which was developed through the observation of its effects on lab rats, showed a decrease in food consumption and an increase in calorie burning in mice that received the treatment. The suppression of ghrelin, a hormone found in the gut, can lessen appetite while boosting metabolism, promoting weight loss. Weight loss surgery, such as gastric bypass surgery, also suppresses ghrelin. This can, in part, explain the successful weight loss that most patients experience after having obesity surgery.
Lab mice that were given the vaccine also showed decreased levels of neuropeptide Y (NPY), which is responsible for increasing the appetite signals in the central nervous system...
“An anti-ghrelin vaccine may become an alternate treatment for obesity, to be used in combination with diet and exercise,” said lead investigator Dr. Mariana Monteiro. In other words, this vaccine may someday be a viable alternative to weight loss surgery.
The vaccine, which was developed through the observation of its effects on lab rats, showed a decrease in food consumption and an increase in calorie burning in mice that received the treatment. The suppression of ghrelin, a hormone found in the gut, can lessen appetite while boosting metabolism, promoting weight loss. Weight loss surgery, such as gastric bypass surgery, also suppresses ghrelin. This can, in part, explain the successful weight loss that most patients experience after having obesity surgery.
Lab mice that were given the vaccine also showed decreased levels of neuropeptide Y (NPY), which is responsible for increasing the appetite signals in the central nervous system...
Obesity: Cysteine Plays a Key Role: Amino Acid May Be at Root of Obesity
People with high levels of the amino acid cysteine carry 6-10 kilograms more fat than other people. Norwegian researchers studying this phenomenon are generating knowledge which could help to prevent and treat life-threatening obesity.
"There is a very high correlation between high levels of cysteine and obesity," explains Professor of Nutrition Helga Refsum of the University of Oslo's Department of Nutrition. The question is whether this is a causal relationship. Is much of the body's fat due to a high cysteine level, and if so, what is the connection? Why do some people have higher cysteine levels than others? How much is owing to genetic factors, and how much is affected by diet?
Researchers are now closing in on some answers. A comprehensive study, funded under the Research Council of Norway's funding scheme for independent basic research (FRIPRO), aims to shed light on the underlying biological mechanism linking cysteine to obesity. The project started up in 2010 and will run until 2013.
Cooperation between Oslo and Oxford
As an outstanding young researcher in Norway in 1998, Helga Refsum was awarded a grant which she used to build up a working relationship with Oxford University and Dr. Amany Elshorbagy. Their collaboration led to the discovery of a connection between cysteine and obesity.
The project has evolved into a close collaboration between the University of Oslo and Oxford University, involving several other research institutions as well.
Affects more than weight
Obesity is caused by the intake of more calories than are burned; any surplus is stored as fat in the body. The concept is a simple one at the general level. But at the molecular level, many more facets to this relationship emerge, making it more difficult to pin down. The long, complex biochemical processes of enzymes converting food to energy and building blocks can be affected by many factors. The same is true for the breakdown of fat.
Professor Refsum's research indicates that cysteine plays a key role in how the body metabolises energy, stores fat, and breaks down fat. In this latest project, the researchers will also study how cysteine affects the brain -- for instance, whether cysteine can influence the feeling of being satiated.
Blame our genes
Our genes play a large part in determining our weight.
"We know there is a strong genetic component to the body's weight and fat content," says Professor Refsum, pointing out that 50-80 per cent of body weight is due to genetic factors. "Look at the difference between males and females! Women always have more body fat than men. Nature intended it this way; this is how it should be."
Body fat percentage varies widely between ethnic groups. Taking these differences into account, health personnel tailor their body mass index (BMI) criteria for obesity to different populations.
Genetic factors are undoubtedly involved in cysteine levels, the professor stresses. Indeed, two known genetic conditions demonstrate a clear relationship.
People with the most common form of a genetic condition known as homocystinuria lack one of the enzymes that convert homocysteine to cysteine. These people have low cysteine levels and are extremely slender. By contrast, people with a different genetic condition, Down's syndrome, have 50% more of that same enzyme than normal- and they also have higher-than-average cysteine levels and tend to be overweight.
Public health focus
The connection between cysteine and obesity-related diseases is a major topic of Professor Refsum's research.
"We particularly want to find out if cysteine is associated with obesity-related morbidity -- the myriad of diseases such as diabetes, cardiovascular diseases and certain types of cancer that are associated with obesity. From a public health perspective, it is this aspect of obesity we need to worry about.
With lowered cysteine, mice shed fat
Professor Refsum and her colleagues have demonstrated that reducing cysteine levels leads to weight loss in mice and rats. With subsequent supplements of cysteine, the weight returns -- along with a higher risk of diabetes...
"There is a very high correlation between high levels of cysteine and obesity," explains Professor of Nutrition Helga Refsum of the University of Oslo's Department of Nutrition. The question is whether this is a causal relationship. Is much of the body's fat due to a high cysteine level, and if so, what is the connection? Why do some people have higher cysteine levels than others? How much is owing to genetic factors, and how much is affected by diet?
Researchers are now closing in on some answers. A comprehensive study, funded under the Research Council of Norway's funding scheme for independent basic research (FRIPRO), aims to shed light on the underlying biological mechanism linking cysteine to obesity. The project started up in 2010 and will run until 2013.
Cooperation between Oslo and Oxford
As an outstanding young researcher in Norway in 1998, Helga Refsum was awarded a grant which she used to build up a working relationship with Oxford University and Dr. Amany Elshorbagy. Their collaboration led to the discovery of a connection between cysteine and obesity.
The project has evolved into a close collaboration between the University of Oslo and Oxford University, involving several other research institutions as well.
Affects more than weight
Obesity is caused by the intake of more calories than are burned; any surplus is stored as fat in the body. The concept is a simple one at the general level. But at the molecular level, many more facets to this relationship emerge, making it more difficult to pin down. The long, complex biochemical processes of enzymes converting food to energy and building blocks can be affected by many factors. The same is true for the breakdown of fat.
Professor Refsum's research indicates that cysteine plays a key role in how the body metabolises energy, stores fat, and breaks down fat. In this latest project, the researchers will also study how cysteine affects the brain -- for instance, whether cysteine can influence the feeling of being satiated.
Blame our genes
Our genes play a large part in determining our weight.
"We know there is a strong genetic component to the body's weight and fat content," says Professor Refsum, pointing out that 50-80 per cent of body weight is due to genetic factors. "Look at the difference between males and females! Women always have more body fat than men. Nature intended it this way; this is how it should be."
Body fat percentage varies widely between ethnic groups. Taking these differences into account, health personnel tailor their body mass index (BMI) criteria for obesity to different populations.
Genetic factors are undoubtedly involved in cysteine levels, the professor stresses. Indeed, two known genetic conditions demonstrate a clear relationship.
People with the most common form of a genetic condition known as homocystinuria lack one of the enzymes that convert homocysteine to cysteine. These people have low cysteine levels and are extremely slender. By contrast, people with a different genetic condition, Down's syndrome, have 50% more of that same enzyme than normal- and they also have higher-than-average cysteine levels and tend to be overweight.
Public health focus
The connection between cysteine and obesity-related diseases is a major topic of Professor Refsum's research.
"We particularly want to find out if cysteine is associated with obesity-related morbidity -- the myriad of diseases such as diabetes, cardiovascular diseases and certain types of cancer that are associated with obesity. From a public health perspective, it is this aspect of obesity we need to worry about.
With lowered cysteine, mice shed fat
Professor Refsum and her colleagues have demonstrated that reducing cysteine levels leads to weight loss in mice and rats. With subsequent supplements of cysteine, the weight returns -- along with a higher risk of diabetes...
Nicotine: A cure for obesity?
Many cigarette smokers have shed extra pounds through their otherwise-unhealthy nicotine habit. But now, scientists have identified and isolated the pathways in the brain that are affected by nicotine's appetite suppressants. The research, published in the journal Science, might lead to the development of a healthy, nicotine-based treatment to control obesity. Here, a short guide to the findings:
How did the researchers make their discovery?
It was accidental, actually. Researchers from Yale and Baylor were looking for new drugs to treat depression, when they noticed that mice given nicotine were eating less. The scientists gave the mice a chemical compound that blocked nicotine receptors, and the rodents' appetites returned. Next, the researchers genetically modified some mice to knock out those nicotine receptors. When given nicotine, the mice without nicotine receptors did not lose weight, but mice with the receptors did. The researchers also found that these receptors are independent from those known to trigger tobacco cravings in smokers...
How did the researchers make their discovery?
It was accidental, actually. Researchers from Yale and Baylor were looking for new drugs to treat depression, when they noticed that mice given nicotine were eating less. The scientists gave the mice a chemical compound that blocked nicotine receptors, and the rodents' appetites returned. Next, the researchers genetically modified some mice to knock out those nicotine receptors. When given nicotine, the mice without nicotine receptors did not lose weight, but mice with the receptors did. The researchers also found that these receptors are independent from those known to trigger tobacco cravings in smokers...
Fat affects brain's ability to control weight: study
The relationship between a high-fat diet and obesity may be more complicated than was previously thought, according to a new study unveiled at the annual meeting of the Endocrine Society in Boston.
Eating fatty foods may injure neurons in an area of the brain that controls body weight, found researchers at the Diabetes and Obesity Center of Excellence at the University of Washington in Seattle.
"The possibility that brain injury may be a consequence of the overconsumption of a typical American diet offers a new explanation for why sustained weight loss is so difficult for most obese individuals to achieve," said presenting author Joshua Thaler.
Researchers studied rats and mice fed a high-fat diet - that is, one with a similar fat content to the average American diet - for periods varying between one day and eight months. A detailed analysis was then carried out on the animals' brains.
Within the first three days on the diet, the rodents were consuming nearly double the daily calories that they usually would...
Eating fatty foods may injure neurons in an area of the brain that controls body weight, found researchers at the Diabetes and Obesity Center of Excellence at the University of Washington in Seattle.
"The possibility that brain injury may be a consequence of the overconsumption of a typical American diet offers a new explanation for why sustained weight loss is so difficult for most obese individuals to achieve," said presenting author Joshua Thaler.
Researchers studied rats and mice fed a high-fat diet - that is, one with a similar fat content to the average American diet - for periods varying between one day and eight months. A detailed analysis was then carried out on the animals' brains.
Within the first three days on the diet, the rodents were consuming nearly double the daily calories that they usually would...
Sunday, June 12, 2011
The RNA roots of obesity?
Two upregulated microRNA molecules may lie at the heart of insulin signalling malfunctions, which can lead to obesity and type 2 diabetes, according to researchers in Switzerland. Scientists at ETH Zurich found that silencing the two microRNAs improved glucose sensitivity in obese mice, and in a paper published today (8 June) in Nature, they suggest that the findings may point the way to potential obesity treatments in humans.
“The effects they are showing are quite striking,” said Phillip Scherer, a fat cell physiologist at the University of Texas Southwestern Medical School, who was not involved in the study. The microRNAs studied in the paper were “so blatantly, obviously up-regulated in the obese state.”...
“The effects they are showing are quite striking,” said Phillip Scherer, a fat cell physiologist at the University of Texas Southwestern Medical School, who was not involved in the study. The microRNAs studied in the paper were “so blatantly, obviously up-regulated in the obese state.”...
Yo-Yo Dieting Healthier Than Obesity?
In a recent study comparing lifelong obesity to the weight fluctuations of "yo-yo dieting," it is suggested that it’s better to attempt to lose weight than to not diet and stay obese.
"It is clear that remaining on a stable, healthy diet provides the best outcome for health and longevity," which the study's principal investigator, Edward List, PhD, a scientist at Ohio University, Athens, was quoted as saying.
"However, obese individuals commonly weight cycle — they have repeated intentional weight loss followed by weight regain, often called yo-yo dieting. While yo-yo dieting is thought to be harmful, there is little hard scientific evidence to support that."
In order to verify the long-term health effects of yo-yo dieting, List and his collaborators performed what they call "the first controlled study of a yo-yo diet regimen used for an entire life span" with the aid of mice...
"It is clear that remaining on a stable, healthy diet provides the best outcome for health and longevity," which the study's principal investigator, Edward List, PhD, a scientist at Ohio University, Athens, was quoted as saying.
"However, obese individuals commonly weight cycle — they have repeated intentional weight loss followed by weight regain, often called yo-yo dieting. While yo-yo dieting is thought to be harmful, there is little hard scientific evidence to support that."
In order to verify the long-term health effects of yo-yo dieting, List and his collaborators performed what they call "the first controlled study of a yo-yo diet regimen used for an entire life span" with the aid of mice...
Study links insulin action on brain's reward circuitry to obesity
Researchers reporting in the June issue of Cell Metabolism, a Cell Press publication, have what they say is some of the first solid proof that insulin has direct effects on the reward circuitry of the brain. Mice whose reward centers can no longer respond to insulin eat more and become obese, they show.
The findings suggest that insulin resistance might help to explain why those who are obese may find it so difficult to resist the temptation of food and take the weight back off...
The findings suggest that insulin resistance might help to explain why those who are obese may find it so difficult to resist the temptation of food and take the weight back off...
Anti-obesity vaccine boosts calorie expenditure, curbs appetite in mice
Diet and exercise that are mainstays for treating and preventing obesity might get a boost from a newly developed anti-obesity vaccine found to curb appetite and boost calorie burning in mice...
Nicotine treatment 'could control obesity'
Scientists have identified a group of neurons in the brain responsible for smokers' lack of appetite.
In an article in the journal Science, Yale University researchers describe experiments on mice which found nicotine activates neurons to send signals the body has had enough to eat.
However they are not the same neurons which trigger a craving for tobacco.
As a result, the researchers say nicotine-based treatments could help control obesity.
A research team from Yale University School of Medicine and Baylor College of Medicine in Houston performed a combination of molecular, pharmacological, behavioural and genetic experiments on mice.
They found that nicotine influences a collection of central nervous system circuits, known as the body's hypothalamic melanocortin system, by activating certain receptors.
These receptors, in turn, increase the activity of pro-opiomelanocortin (POMC) neurons, known for their effects on obesity in humans and animals.
Targeting cells
When subjected to nicotine, mice lacking the POMC pathway did not lose weight, but mice with the pathway did...
In an article in the journal Science, Yale University researchers describe experiments on mice which found nicotine activates neurons to send signals the body has had enough to eat.
However they are not the same neurons which trigger a craving for tobacco.
As a result, the researchers say nicotine-based treatments could help control obesity.
A research team from Yale University School of Medicine and Baylor College of Medicine in Houston performed a combination of molecular, pharmacological, behavioural and genetic experiments on mice.
They found that nicotine influences a collection of central nervous system circuits, known as the body's hypothalamic melanocortin system, by activating certain receptors.
These receptors, in turn, increase the activity of pro-opiomelanocortin (POMC) neurons, known for their effects on obesity in humans and animals.
Targeting cells
When subjected to nicotine, mice lacking the POMC pathway did not lose weight, but mice with the pathway did...
Wednesday, June 08, 2011
Adding Tangerines to Your Weight Loss Diet Plan
A recent study based out of the University of Ontario has found that a certain substance found in tangerines has been crucial in preventing obesity in mice. Not only that, but it also helped to protect them from Type 2 Diabetes, another disease also associated with obesity...
Thursday, May 26, 2011
Weight Gain – Brain Protein Found To Contribute To Obesity
Weizmann Institute scientists have added another piece to the obesity puzzle, showing how and why a certain protein that is active in a small part of the brain contributes to weight gain. This research appeared today in Cell Metabolism.
Prof. Ari Elson and his team in the Institute’s Molecular Genetics Department made the discovery when working with female mice that were genetically engineered to lack this protein, called protein tyrosine phosphatase epsilon (PTPe, for short). The scientists had originally intended to investigate osteoporosis, and thus, they also removed the ovaries of these mice. Taking out ovaries typically causes mice to gain weight to the point of obesity – so the scientists were surprised to find that the weight of the genetically-engineered mice remained stable. Working with Dr. Alon Chen and his group in the Neurobiology Department and Prof. Hilla Knobler, Head of the Unit of Metabolic Disease and Diabetes of Kaplan Medical Center, the researchers fed these mice a high-fat diet, yet the PTPe-deficient mice maintained their svelte figures; they burned more energy and had more stable glucose levels as well.
To find out how the lack of this protein could keep mice slim and healthy, the scientists looked at the hypothalamus, a region of the brain that takes in assorted stimuli, including a wide variety of hormones, and sends out messages of its own in the form of new hormones and nerve signals. The hypothalamus plays a vital role in regulating body mass – a complex balancing act that involves, among other things, controlling appetite and physical activity...
Prof. Ari Elson and his team in the Institute’s Molecular Genetics Department made the discovery when working with female mice that were genetically engineered to lack this protein, called protein tyrosine phosphatase epsilon (PTPe, for short). The scientists had originally intended to investigate osteoporosis, and thus, they also removed the ovaries of these mice. Taking out ovaries typically causes mice to gain weight to the point of obesity – so the scientists were surprised to find that the weight of the genetically-engineered mice remained stable. Working with Dr. Alon Chen and his group in the Neurobiology Department and Prof. Hilla Knobler, Head of the Unit of Metabolic Disease and Diabetes of Kaplan Medical Center, the researchers fed these mice a high-fat diet, yet the PTPe-deficient mice maintained their svelte figures; they burned more energy and had more stable glucose levels as well.
To find out how the lack of this protein could keep mice slim and healthy, the scientists looked at the hypothalamus, a region of the brain that takes in assorted stimuli, including a wide variety of hormones, and sends out messages of its own in the form of new hormones and nerve signals. The hypothalamus plays a vital role in regulating body mass – a complex balancing act that involves, among other things, controlling appetite and physical activity...
Mice to reveal key to human obesity
Call him fatso, if you will. And call her a lazy lump if that is what you wish. But the big fat mice and their ilk which live in an exclusive `colony of mice' at a laboratory at Tarnaka will soon reveal to the world what makes them so obese. And here's why what they reveal will be important for the world.
After 14 years of research, scientists at the National Centre for Laboratory Animal Sciences (NCLAS) at the National Insitute of Nutrition (NIN) at Tarnaka are on the verge of a major breakthrough in detecting what makes the experimental breed of mice obese.
The breakthrough will be significant for the world as it will help fight obesity in human beings. Further studies based on the findings in the obese mice will reveal what makes human beings also obese. Obesity is enemy no. 1 in human beings and most diseases are directly related to the problem.
After 14 years of research, scientists at the National Centre for Laboratory Animal Sciences (NCLAS) at the National Insitute of Nutrition (NIN) at Tarnaka are on the verge of a major breakthrough in detecting what makes the experimental breed of mice obese.
The breakthrough will be significant for the world as it will help fight obesity in human beings. Further studies based on the findings in the obese mice will reveal what makes human beings also obese. Obesity is enemy no. 1 in human beings and most diseases are directly related to the problem.
Sunday, May 08, 2011
Silencing a protein could turn fat cells into energy burners in individuals at risk for type 2 diabetes
Silencing the neuropeptide Y (NPY) protein in the brain may turn adipose tissue into a type of fat that burns excess energy rather than storing it, according to a new study from Johns Hopkins University researchers. The findings could have major implications for obese individuals who are at risk for developing type 2 diabetes.
Most adipose tissue in the body is known as white fat. This material is what the body uses to store excess energy and is typically located around the midsection. High levels of this fat have been shown to increase an individual’s risk of chronic diseases, such as heart disease and type 2 diabetes.
However, there is another type of adipose tissue that serves a very different function. Brown fat instructs the body to burn unneeded calories. Most adults have very little of this tissue.
Yet it may be possible for individuals to develop more. The researchers reported in the journal Cell Metabolism that silencing the NPY protein in the brain turns typical white fat cells into energy-burning brown adipose tissue.
The team began experimenting with switching off the expression of NPY protein in laboratory mice because it had previously been shown to mediate feelings of hunger and thirst. They speculated that by silencing the protein, mice would want to eat less. As expected, their study showed that this was the case. However, more surprisingly, mice that lacked expression of the NPY protein also had considerably more brown fat...
Most adipose tissue in the body is known as white fat. This material is what the body uses to store excess energy and is typically located around the midsection. High levels of this fat have been shown to increase an individual’s risk of chronic diseases, such as heart disease and type 2 diabetes.
However, there is another type of adipose tissue that serves a very different function. Brown fat instructs the body to burn unneeded calories. Most adults have very little of this tissue.
Yet it may be possible for individuals to develop more. The researchers reported in the journal Cell Metabolism that silencing the NPY protein in the brain turns typical white fat cells into energy-burning brown adipose tissue.
The team began experimenting with switching off the expression of NPY protein in laboratory mice because it had previously been shown to mediate feelings of hunger and thirst. They speculated that by silencing the protein, mice would want to eat less. As expected, their study showed that this was the case. However, more surprisingly, mice that lacked expression of the NPY protein also had considerably more brown fat...
Researchers Suggest Role for Hypothalamic PPAR-Gamma in Diabetes Drug-Related Weight Gain
Two separate research teams claim that activity of nuclear receptor peroxisome proliferator-activated receptor-γ (PPAR-γ) in the brain plays a role in the mechanisms that cause weight gain among patients receiving thiazolidinedione (TZD) treatment for type 2 diabetes. The two sets of animal-based research, one led by a team at the University of California, San Diego (UCSD), and the other carried out by scientists at the University of Cincinnati College of Medicine, have identified a previously unknown role for central nervous system PPAR-γ in the regulation of energy balance, leptin sensitivity, and at least some of the weight gain associated with administering PPAR-γ–modulating drugs. Both research teams published their results in Nature Medicine...
To investigate this possibility further, Jerrold M. Olefsky, Ph.D., at UCSD’s Department of Medicine, and colleagues, generated mice in which the gene for PPAR-γ was knocked out only in the brain (Pparg brain knockout [BKO] mice), to determine whether neuronal PPAR-γ signalling contributes to either weight gain or insulin sensitivity...
Studies by Dr. Seeley’s team also concurred with those of the UCSD team with regard to the effects of CNS PPAR-γ on leptin signalling. Leptin signalling in the hypothalamus is blunted in rats fed a HFD, and this leptin resistance is thought to contribute to the continued accumulation of body fat. The Cincinnati team hypothesized that hypothalamic PPAR-γ specifically may contribute to the development of HFD-induced leptin resistance, and that chronic antagonism of CNS PPAR-γ would restore leptin sensitivity these animals. To test this, they administered the PPAR-γ antagonist into the lateral ventricle of HFD-fed rats, at a dose that had no effect on body weight but that did result in significantly lower hypothalamic expression of PPAR-γ’s target gene lipoprotein lipase...
To investigate this possibility further, Jerrold M. Olefsky, Ph.D., at UCSD’s Department of Medicine, and colleagues, generated mice in which the gene for PPAR-γ was knocked out only in the brain (Pparg brain knockout [BKO] mice), to determine whether neuronal PPAR-γ signalling contributes to either weight gain or insulin sensitivity...
Studies by Dr. Seeley’s team also concurred with those of the UCSD team with regard to the effects of CNS PPAR-γ on leptin signalling. Leptin signalling in the hypothalamus is blunted in rats fed a HFD, and this leptin resistance is thought to contribute to the continued accumulation of body fat. The Cincinnati team hypothesized that hypothalamic PPAR-γ specifically may contribute to the development of HFD-induced leptin resistance, and that chronic antagonism of CNS PPAR-γ would restore leptin sensitivity these animals. To test this, they administered the PPAR-γ antagonist into the lateral ventricle of HFD-fed rats, at a dose that had no effect on body weight but that did result in significantly lower hypothalamic expression of PPAR-γ’s target gene lipoprotein lipase...
Protein Contributes to Obesity
Weizmann Institute scientists have added another piece to the obesity puzzle, showing how and why a certain protein that is active in a small part of the brain contributes to weight gain. This research appeared in Cell Metabolism.
Prof. Ari Elson and his team in the Institute’s Molecular Genetics Department made the discovery when working with female mice that were genetically engineered to lack this protein, called protein tyrosine phosphatase epsilon (PTPe, for short). The scientists had originally intended to investigate osteoporosis, and thus, they also removed the ovaries of these mice. Taking out ovaries typically causes mice to gain weight to the point of obesity – so the scientists were surprised to find that the weight of the genetically-engineered mice remained stable. Working with Dr. Alon Chen and his group in the Neurobiology Department and Prof. Hilla Knobler, Head of the Unit of Metabolic Disease and Diabetes of Kaplan Medical Center, the researchers fed these mice a high-fat diet, yet the PTPe-deficient mice maintained their svelte figures; they burned more energy and had more stable glucose levels as well...
Prof. Ari Elson and his team in the Institute’s Molecular Genetics Department made the discovery when working with female mice that were genetically engineered to lack this protein, called protein tyrosine phosphatase epsilon (PTPe, for short). The scientists had originally intended to investigate osteoporosis, and thus, they also removed the ovaries of these mice. Taking out ovaries typically causes mice to gain weight to the point of obesity – so the scientists were surprised to find that the weight of the genetically-engineered mice remained stable. Working with Dr. Alon Chen and his group in the Neurobiology Department and Prof. Hilla Knobler, Head of the Unit of Metabolic Disease and Diabetes of Kaplan Medical Center, the researchers fed these mice a high-fat diet, yet the PTPe-deficient mice maintained their svelte figures; they burned more energy and had more stable glucose levels as well...
Monday, May 02, 2011
Eat breakfast to prevent metabolic syndrome
Higher fat at breakfast may be healthier than you think, concludes a new University of Alabama at Birmingham (UAB) study.
According to researchers, the adage "Eat breakfast like a king, lunch like a prince and dinner like a pauper" can be the best advice to follow to prevent metabolic syndrome.
Metabolic syndrome is characterized by abdominal obesity, high triglycerides, insulin resistance and other cardiovascular disease-risk factors.
To reach the conclusion, boffins examined the influence exerted by the type of foods and specific timing of intake on the development of metabolic syndrome characteristics in mice.
The UAB research revealed that mice fed a meal higher in fat after waking had normal metabolic profiles. In contrast, mice that ate a more carbohydrate-rich diet in the morning and consumed a high-fat meal at the end of the day saw increased weight gain, adiposity, glucose intolerance and other markers of the metabolic syndrome...
According to researchers, the adage "Eat breakfast like a king, lunch like a prince and dinner like a pauper" can be the best advice to follow to prevent metabolic syndrome.
Metabolic syndrome is characterized by abdominal obesity, high triglycerides, insulin resistance and other cardiovascular disease-risk factors.
To reach the conclusion, boffins examined the influence exerted by the type of foods and specific timing of intake on the development of metabolic syndrome characteristics in mice.
The UAB research revealed that mice fed a meal higher in fat after waking had normal metabolic profiles. In contrast, mice that ate a more carbohydrate-rich diet in the morning and consumed a high-fat meal at the end of the day saw increased weight gain, adiposity, glucose intolerance and other markers of the metabolic syndrome...
Nutrient in tangerines shown to limit type 2 diabetes risk
The antioxidant nobiletin, which occurs naturally in high levels in tangerines, may help individuals avoid the symptoms of metabolic syndrome and prevent them from developing type 2 diabetes, according to a new study from a group of University of Western Ontario researchers.
Their study, which was published in the journal Diabetes, showed that the molecule prevented mice from experiencing elevated cholesterol levels, high blood pressure, impaired glucose tolerance, buildups of fat in the liver and excess weight gain, even when they were fed a high-fat diet. The mice also showed no signs of type 2 diabetes...
Their study, which was published in the journal Diabetes, showed that the molecule prevented mice from experiencing elevated cholesterol levels, high blood pressure, impaired glucose tolerance, buildups of fat in the liver and excess weight gain, even when they were fed a high-fat diet. The mice also showed no signs of type 2 diabetes...
Saturday, April 30, 2011
Melatonin Might Help Control Weight Gain and Prevent Heart Disease Associated With Obesity
University of Granada researchers have shown that melatonin -- a natural hormone produced by the body -- helps in controlling weight gain, even without reducing the intake of food. Melatonin also improves blood lipid profile, as it reduces triglicerids, and also increases HDL cholesterol and reduces LDL cholesterol.
Melatonin is found in small quantities in some fruits and vegetables as mustard, Goji berries, almonds, sunflower seeds, cardamom, fennel, coriander and cherries. Thus, the intake of this kind of food might help in controlling weight gain and preventing heart diseases associated to obesity and dyslipidemia.
Trials with rats
University of Granada researchers have analyzed in young Zucker diabetic obese rats the effects of melatonin on obesity, dyslipidemia and high blood pressure associated with obesity. Melatonin was found to be beneficial for young rats that had not still developed any metabolic or heart disease. Researchers think that melatonin might help prevent heart disease associated with obesity and dyslipidemia...
Melatonin is found in small quantities in some fruits and vegetables as mustard, Goji berries, almonds, sunflower seeds, cardamom, fennel, coriander and cherries. Thus, the intake of this kind of food might help in controlling weight gain and preventing heart diseases associated to obesity and dyslipidemia.
Trials with rats
University of Granada researchers have analyzed in young Zucker diabetic obese rats the effects of melatonin on obesity, dyslipidemia and high blood pressure associated with obesity. Melatonin was found to be beneficial for young rats that had not still developed any metabolic or heart disease. Researchers think that melatonin might help prevent heart disease associated with obesity and dyslipidemia...
Monday, April 25, 2011
Type 2 diabetes, like Type 1, may be an autoimmune disease, researchers say
Type 2 diabetes, like Type 1, may be an autoimmune disease, but the immune system's target cells are different, Stanford researchers said Sunday. The discovery sheds new light on how obesity contributes to the onset of Type 2 diabetes and could lead to new types of treatment for the disorder, the researchers reported in the journal Nature Medicine.
Diabetes is a growing problem in the United States, triggered in large part by the obesity epidemic. An estimated 27 million Americans are now thought to have diabetes, with the vast majority of them -- all but about a million -- afflicted with Type 2 diabetes. That disorder strikes in adulthood and is marked by a growing inability of cells to respond to insulin in the bloodstream, which necessitates using drugs to increase the output of the hormone by the pancreas. Intriguingly, not everyone who becomes obese develops diabetes, however, and researchers have never been sure why.
Dr. Daniel Winer, an endocrine pathologist now at the University of Toronto, and his twin, Dr. Shawn Winer of the University of Toronto's Hospital for Sick Children, reasoned that the death of excess fat cells might trigger an autoimmune reaction. In an earlier study with senior author Dr. Edgar Engleman of the Stanford University School of Medicine, they demonstrated in mice that, as fat accumulates in the tissues surrounding organs, it outstrips its blood supply, leading to the death of cells on the periphery of the fat deposits. When that occurs, the body mobilizes its immune system to break down and carry off the dead cells. But that produces antibodies against the cells and many of the proteins normally found only inside the cells.
In the new study, the team turned its attention to B cells, the lymphocytes or white blood cells that manufacture antibodies against foreign invaders. They genetically engineered mice so that they could not produce B cells and found that the rodents never became diabetic, no matter how fat they became. They next looked at normal mice that were prone to becoming diabetic when they became obese. One group they treated with a biological drug called anti-CD20 that binds to B cells and blocks their activity. The second group received no treatment. The mice that received the drug did not become diabetic when they became obese, while those that did not receive it did become diabetic. The effect lasted only about 40 days, however, and then needed to be repeated...
Diabetes is a growing problem in the United States, triggered in large part by the obesity epidemic. An estimated 27 million Americans are now thought to have diabetes, with the vast majority of them -- all but about a million -- afflicted with Type 2 diabetes. That disorder strikes in adulthood and is marked by a growing inability of cells to respond to insulin in the bloodstream, which necessitates using drugs to increase the output of the hormone by the pancreas. Intriguingly, not everyone who becomes obese develops diabetes, however, and researchers have never been sure why.
Dr. Daniel Winer, an endocrine pathologist now at the University of Toronto, and his twin, Dr. Shawn Winer of the University of Toronto's Hospital for Sick Children, reasoned that the death of excess fat cells might trigger an autoimmune reaction. In an earlier study with senior author Dr. Edgar Engleman of the Stanford University School of Medicine, they demonstrated in mice that, as fat accumulates in the tissues surrounding organs, it outstrips its blood supply, leading to the death of cells on the periphery of the fat deposits. When that occurs, the body mobilizes its immune system to break down and carry off the dead cells. But that produces antibodies against the cells and many of the proteins normally found only inside the cells.
In the new study, the team turned its attention to B cells, the lymphocytes or white blood cells that manufacture antibodies against foreign invaders. They genetically engineered mice so that they could not produce B cells and found that the rodents never became diabetic, no matter how fat they became. They next looked at normal mice that were prone to becoming diabetic when they became obese. One group they treated with a biological drug called anti-CD20 that binds to B cells and blocks their activity. The second group received no treatment. The mice that received the drug did not become diabetic when they became obese, while those that did not receive it did become diabetic. The effect lasted only about 40 days, however, and then needed to be repeated...
Scientists find treatment for hypertension, obesity
South Korean scientists said Thursday they have found a treatment material that may help people to better deal with hypertension, obesity, and high blood fat.
Researchers led by Lee Chul-ho at the Korea Research Institute of Bioscience and Biotechnology (KRIBB) claimed they isolated a new material called MB12066 that showed promising results in animal tests.
Hypertension currently affects 30 percent of South Korea’s population with the local drug market standing at 1.4 trillion won ($1.3 billion).
“Mice engineered to have high blood pressure and given the MB12066 for six straight weeks showed marked improvements compared to other animals not administered with the new target material,” Lee said...
Researchers led by Lee Chul-ho at the Korea Research Institute of Bioscience and Biotechnology (KRIBB) claimed they isolated a new material called MB12066 that showed promising results in animal tests.
Hypertension currently affects 30 percent of South Korea’s population with the local drug market standing at 1.4 trillion won ($1.3 billion).
“Mice engineered to have high blood pressure and given the MB12066 for six straight weeks showed marked improvements compared to other animals not administered with the new target material,” Lee said...
Friday, April 22, 2011
Nobiletin in Tangerines: Better Solution to Obesity and Heart Diseases, Study
Scientists have identified one more superfood. They argue that the fruit like tangerine, which is quite popular among kids, can be very useful and healthy for adults. Especially for those who have diseases related to heart and obesity.
Researchers from the University of Western Ontario, maintain that nobiletin - a substance contained in tangerine peel is ten times potent than the one found in pigment found in the peel of grapefruit. And although the therapeutic effect of citrus has only been proved in mice...
Researchers from the University of Western Ontario, maintain that nobiletin - a substance contained in tangerine peel is ten times potent than the one found in pigment found in the peel of grapefruit. And although the therapeutic effect of citrus has only been proved in mice...
MU professor finds plant oil could help to combat obesity
Jim Perfield has scattered Post-it notes around his desk with scientific health questions he'd like to tackle. He's starting with obesity.
An MU assistant professor in the departments of nutrition and exercise physiology and food science, Perfield, 33, said he is trying to better understand the relationship between nutrition and obesity.
He has conducted research on a plant oil with the potential to reduce stomach fat by inhibiting an enzyme involved in the metabolism of fatty acids.
It could be used not only to achieve a tighter stomach but also to avoid a number of health issues associated with obesity, such as diabetes, heart disease and liver problems.
Sterculic oil was fed to rats as part of their diet, and Perfield found rats who consumed the oil ended up with less belly or "intra-abdominal" fat than rats who weren't given the oil.
Perfield and his lab conducted the experiments with a breed of Japanese rats prone to obesity...
An MU assistant professor in the departments of nutrition and exercise physiology and food science, Perfield, 33, said he is trying to better understand the relationship between nutrition and obesity.
He has conducted research on a plant oil with the potential to reduce stomach fat by inhibiting an enzyme involved in the metabolism of fatty acids.
It could be used not only to achieve a tighter stomach but also to avoid a number of health issues associated with obesity, such as diabetes, heart disease and liver problems.
Sterculic oil was fed to rats as part of their diet, and Perfield found rats who consumed the oil ended up with less belly or "intra-abdominal" fat than rats who weren't given the oil.
Perfield and his lab conducted the experiments with a breed of Japanese rats prone to obesity...
Blueberries May Help Fight Obesity, Study Finds
Blueberries have been shown to have a positive effect on everything from cardiovascular health to aging, and now it seems that eating these berries could help you slim down as well.
Shiwani Moghe, a researcher from Texas Woman’s University in Denton, Texas, looked at whether blueberries and their high polyphenol content could play a role in fighting obesity.
In a study of tissue cultures taken from mice, Moghe examined what effect the polyphenols in the berries have in fighting the development of fats cells, and what she found was the highest dose of polyphenols cut the number of fat cells by 73 percent, while the smallest dose showed a 27 percent decrease...
Shiwani Moghe, a researcher from Texas Woman’s University in Denton, Texas, looked at whether blueberries and their high polyphenol content could play a role in fighting obesity.
In a study of tissue cultures taken from mice, Moghe examined what effect the polyphenols in the berries have in fighting the development of fats cells, and what she found was the highest dose of polyphenols cut the number of fat cells by 73 percent, while the smallest dose showed a 27 percent decrease...
Monday, April 11, 2011
Dyslipidemia Metabolic Signaling Pathway Identified By Researchers
Dyslipidemia's metabolic signaling pathway, a nutrient sensing pathway which is involved in the disruption of cellular lipid homeostasis, has been identified by researchers.
The researchers from Boston University School of Medicine (BUSM), including Yu Li, PhD, and other colleagues, used obese and insulin-resistant mice who were fed a diet high in fat and sucrose, reports PhysOrg.com.
This pathway may also have implications for the health benefits of polyphenols-containing foods against fatty liver, hyperlipidemia, and atherosclerosis associated with obesity and type 2 diabetes...
The researchers from Boston University School of Medicine (BUSM), including Yu Li, PhD, and other colleagues, used obese and insulin-resistant mice who were fed a diet high in fat and sucrose, reports PhysOrg.com.
This pathway may also have implications for the health benefits of polyphenols-containing foods against fatty liver, hyperlipidemia, and atherosclerosis associated with obesity and type 2 diabetes...
Researchers Identify Micro-RNA That Regulates Insulin in Obesity
Scientists at the Max Planck Institute for Neurological Research in Cologne and the Cologne Cluster of Excellence in Cellular Stress Responses in Aging-associated Diseases (CECAD) discovered that obese mice form increased levels of the regulatory RNA molecule miRNA-143.miRNA-143 inhibits the insulin-stimulated activation of the enzyme AKT.
Without active AKT, insulin cannot unfold its blood-sugar-reducing effect and the blood sugar level is thrown out of kilter...
Without active AKT, insulin cannot unfold its blood-sugar-reducing effect and the blood sugar level is thrown out of kilter...
Tangerines May Prevent Obesity, Diabetes
Tangerines may prevent obesity and protect against heart disease, Type 2 diabetes, and other metabolic conditions, according to a new study published in the journal Diabetes.
A flavinoid in tangerines called Nobiletin was found to be specifically linked to the effects.
The researchers studied mice that were fed a high fat, high-sugar diet. The control group suffered from elevated cholesterol, high and glucose levels, fatty liver, and other signs of metabolic syndrome. These conditions cause a greater risk of Type 2 diabetes and cardiovascular disease.
Meanwhile the mice who received the Nobiletin did not suffer from these conditions. The substance was shown to prevent fat buildup in the liver by stimulating the gene expression involved in burning extra fat, meanwhile inhibiting genes that create fat.
"The Nobiletin-treated mice were basically protected from obesity," said Murray Huff, the Director of the Vascular Biology Research Group at Robarts...
A flavinoid in tangerines called Nobiletin was found to be specifically linked to the effects.
The researchers studied mice that were fed a high fat, high-sugar diet. The control group suffered from elevated cholesterol, high and glucose levels, fatty liver, and other signs of metabolic syndrome. These conditions cause a greater risk of Type 2 diabetes and cardiovascular disease.
Meanwhile the mice who received the Nobiletin did not suffer from these conditions. The substance was shown to prevent fat buildup in the liver by stimulating the gene expression involved in burning extra fat, meanwhile inhibiting genes that create fat.
"The Nobiletin-treated mice were basically protected from obesity," said Murray Huff, the Director of the Vascular Biology Research Group at Robarts...
Saturday, April 02, 2011
Micro-RNA Blocks The Effect Of Insulin In Obesity
Max Planck researchers have discovered a new mechanism that leads to the development of type 2 diabetes in obesity. Body weight influences the risk of developing diabetes: between 80 and 90 percent of patients with type 2 diabetes are overweight or obese. According to scientists at the Max Planck Institute for Neurological Research in Cologne and the Cologne Cluster of Excellence in Cellular Stress Responses in Aging-associated Diseases (CECAD), short ribonucleic acid molecules, known as micro-RNAs, appear to play an important role in this mechanism.
The researchers discovered that the obese mice form increased levels of the regulatory RNA molecule miRNA-143. miRNA-143 inhibits the insulin-stimulated activation of the enzyme AKT. Without active AKT, insulin cannot unfold its blood-sugar-reducing effect and the blood sugar level is thrown out of kilter. This newly discovered mechanism could provide the starting point for the development of new drugs for the treatment of diabetes...
The researchers discovered that the obese mice form increased levels of the regulatory RNA molecule miRNA-143. miRNA-143 inhibits the insulin-stimulated activation of the enzyme AKT. Without active AKT, insulin cannot unfold its blood-sugar-reducing effect and the blood sugar level is thrown out of kilter. This newly discovered mechanism could provide the starting point for the development of new drugs for the treatment of diabetes...
Sunday, March 27, 2011
Junk food mums have junk food babies
A new study involving rats suggests that pregnant and breastfeeding women who indulge in high levels of fat and sugar are likely to have children who indulge in the same types of food.
According to the research, this happens because the high fat and high sugar diet leads to changes in the fetal brain's reward pathway, altering food preferences...
According to the research, this happens because the high fat and high sugar diet leads to changes in the fetal brain's reward pathway, altering food preferences...
Pollution Links to Obesity and Diabetes
Ohio State University has a new research revealed in the United States that childhood exposure to common air pollutants increases the risk in obesity and developing diabetes. Daily Express reported that those who are brought up in the city and are exposed to microscopic pollutants from car exhaust and burning fuels can lead to gaining weight in youngsters.
Researchers also discovered that pollutants can also increase the risk of developing of diabetes by increasing the insulin resistant of the individual. The results that have been shown are based on the tests done on mice and the pollution levels that match to the level on urban areas. A group of baby mice was been exposed to microscopic pollution while the other group of baby mice were exposed to a filtered air. The age of the mice was according to the age of toddlers and to late adolescent humans. Mice from both group were fed normal or in a high fat diet.
On the study, the animals on a high fat diet gained weight while the other group that exposed to the atmospheric pollutants have elevated levels of blood sugar. Researchers found out that they have also high level of insulin resistance and high level of fat on their abdomen and on their internal organs.
Mice on a high fat diet who breathed in toxic air did not increase their weight than those who are in high fat diet exposed to fresh air. Mice that been exposed to pollutants with a normal diet have increased level of body fat. This suggests that the exposure to pollutants would trigger to weight gain...
Researchers also discovered that pollutants can also increase the risk of developing of diabetes by increasing the insulin resistant of the individual. The results that have been shown are based on the tests done on mice and the pollution levels that match to the level on urban areas. A group of baby mice was been exposed to microscopic pollution while the other group of baby mice were exposed to a filtered air. The age of the mice was according to the age of toddlers and to late adolescent humans. Mice from both group were fed normal or in a high fat diet.
On the study, the animals on a high fat diet gained weight while the other group that exposed to the atmospheric pollutants have elevated levels of blood sugar. Researchers found out that they have also high level of insulin resistance and high level of fat on their abdomen and on their internal organs.
Mice on a high fat diet who breathed in toxic air did not increase their weight than those who are in high fat diet exposed to fresh air. Mice that been exposed to pollutants with a normal diet have increased level of body fat. This suggests that the exposure to pollutants would trigger to weight gain...
Is bacterial chatter behind mental illness, obesity?
The chatter between bugs present in your gut and your brain plays a key role in bringing on psychiatric illness, intestinal diseases and obesity among others.
This 'communication of the body and the brain influence metabolic disorders, such as obesity and diabetes', says Jane Foster, associate professor in psychiatry and behavioural neurosciences at McMaster University.
'We have a hypothesis in my lab that the state of your immune system and your gut bacteria - which are in constant communication - influences your personality,' Foster said.
Using germ-free mice, Foster's research shows gut bugs influence how the brain is wired for learning and memory, the journal Neurogastroenterology and Motility reports...
This 'communication of the body and the brain influence metabolic disorders, such as obesity and diabetes', says Jane Foster, associate professor in psychiatry and behavioural neurosciences at McMaster University.
'We have a hypothesis in my lab that the state of your immune system and your gut bacteria - which are in constant communication - influences your personality,' Foster said.
Using germ-free mice, Foster's research shows gut bugs influence how the brain is wired for learning and memory, the journal Neurogastroenterology and Motility reports...
Maternal Obesity May Lead To Infertility In The Next Generation
Levels of the hormone ghrelin are low in obese women and a recent study accepted for publication in Endocrinology, a publication of The Endocrine Society, reports that mice whose mothers had low ghrelin levels were less fertile due to a defect in implantation...
Wednesday, March 09, 2011
In The Dark Horizon Of Obesity And Diabetes, Klotho Brings A Ray Of Hope
An important discovery in mice may make a big difference in people's waistlines thanks to a team of Harvard scientists who found that reducing the function of a transmembrane protein, called Klotho, in obese mice with high blood sugar levels produced lean mice with reduced blood sugar levels. This protein also exists in humans, suggesting that selectively targeting Klotho could lead to a new class of drugs to reduce obesity and possibly Type 2 diabetes for people. This finding was recently published online in The FASEB Journal.
"Our study is a small step toward reducing the sufferings of obese and diabetic individuals to bring back the joy of healthy life," said M. Shawkat Razzaque, M.D., Ph.D., a researcher involved in the work from the Department of Oral Medicine, Infection and Immunity at Harvard School of Dental Medicine in Boston. "In the dark horizon of obesity and diabetes, Klotho brings a ray of hope."
To make this discovery, Razzaque and colleagues fed increased amounts of food to leptin-deficient mice with the Klotho protein which caused obesity with high blood sugar levels. A second set of mice was bred that was both leptin- and Klotho-deficient, and was fed the same diet as the first set. The second set of mice was lean and had low blood sugar levels, suggesting that reduced Klotho function may not only diminish obesity, but also decrease blood sugar levels. Furthermore, mice without Klotho function gained no body weight after eating a high-fat diet, while mice with functioning Klotho proteins gained body weight following a high-fat diet.
"In Greek mythology, Klotho was the youngest of three fates, the one responsible for spinning the thread of life; since then we have learned that obesity cuts the thread short," said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. "It's good to know that the new molecular biology of Klotho points to agents that will keep us fit and well-spun."...
"Our study is a small step toward reducing the sufferings of obese and diabetic individuals to bring back the joy of healthy life," said M. Shawkat Razzaque, M.D., Ph.D., a researcher involved in the work from the Department of Oral Medicine, Infection and Immunity at Harvard School of Dental Medicine in Boston. "In the dark horizon of obesity and diabetes, Klotho brings a ray of hope."
To make this discovery, Razzaque and colleagues fed increased amounts of food to leptin-deficient mice with the Klotho protein which caused obesity with high blood sugar levels. A second set of mice was bred that was both leptin- and Klotho-deficient, and was fed the same diet as the first set. The second set of mice was lean and had low blood sugar levels, suggesting that reduced Klotho function may not only diminish obesity, but also decrease blood sugar levels. Furthermore, mice without Klotho function gained no body weight after eating a high-fat diet, while mice with functioning Klotho proteins gained body weight following a high-fat diet.
"In Greek mythology, Klotho was the youngest of three fates, the one responsible for spinning the thread of life; since then we have learned that obesity cuts the thread short," said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. "It's good to know that the new molecular biology of Klotho points to agents that will keep us fit and well-spun."...
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