Monday, February 20, 2012
Lipid Sensor GPR120 Linked to Obesity in Mice and Humans
A protein that acts as a lipid sensor, GPR120, can lead to obesity when defective in mice and humans, according to a study published online Feb. 19 in Nature...
Sunday, February 12, 2012
Four Natural Extracts With Anti-Obesity Effects Tested On Rats
University of Granada researchers have identified four plant extracts that might help in preventing and fighting obesity. The researchers identified the most effective plant extracts through in vitro assays; subsequently, extracts were tested on rats. While the results obtained are promising, further studies on animals are required to evaluate and confirm the anti-obesity effects of these extracts. Once their anti-obesity effects are confirmed on animals, the extracts will be tested on humans...
Saturday, February 11, 2012
NIH grant targets inflammation in link between obesity and disease
Preliminary results in mice point way to a potential treatment
If you are obese, you are at great risk of developing heart disease and diabetes. But research now underway at Eastern Virginia Medical School could drastically improve your odds of avoiding these serious diseases.
EVMS has secured a major, five-year research grant from the National Institutes of Health that may lead to ways to prevent the development of these diseases linked to obesity. The $1.8 million grant supports a multidisciplinary study of how to safely thwart chronic inflammation; scientists believe that inflammation triggers disease in people who are overweight.
"Inflammation is key to why central 'belly' fat leads to high risks for diabetes, heart disease and maybe even some forms of cancer," says Jerry L. Nadler, MD, director of the EVMS Strelitz Diabetes Center and principal investigator on the grant.
Inflammation is vital to our health. The immune system uses acute inflammation to battle certain infections and heal wounds; it subsides when no longer needed. But chronic inflammation can cause problems. It is this long-term inflammation that Dr. Nadler and his colleagues are targeting.
Obesity — now at epidemic levels in the United Sates — represents a major public-health challenge for the nation. The risk of having a heart attack triples during obesity. Nearly 80 percent of people who develop type 2 diabetes (often as a result of obesity) also develop heart disease...
If you are obese, you are at great risk of developing heart disease and diabetes. But research now underway at Eastern Virginia Medical School could drastically improve your odds of avoiding these serious diseases.
EVMS has secured a major, five-year research grant from the National Institutes of Health that may lead to ways to prevent the development of these diseases linked to obesity. The $1.8 million grant supports a multidisciplinary study of how to safely thwart chronic inflammation; scientists believe that inflammation triggers disease in people who are overweight.
"Inflammation is key to why central 'belly' fat leads to high risks for diabetes, heart disease and maybe even some forms of cancer," says Jerry L. Nadler, MD, director of the EVMS Strelitz Diabetes Center and principal investigator on the grant.
Inflammation is vital to our health. The immune system uses acute inflammation to battle certain infections and heal wounds; it subsides when no longer needed. But chronic inflammation can cause problems. It is this long-term inflammation that Dr. Nadler and his colleagues are targeting.
Obesity — now at epidemic levels in the United Sates — represents a major public-health challenge for the nation. The risk of having a heart attack triples during obesity. Nearly 80 percent of people who develop type 2 diabetes (often as a result of obesity) also develop heart disease...
Study Unlocks Secrets of Red Wine Chemical
If you love to sit back and sip a glass of cabernet or pinot noir, you can feel good knowing that the health benefits of red wine are now a little less mysterious. Scientists have uncovered how resveratrol, the chemical found in grape skins, peanuts and dark chocolate, works in mice to help fight several chronic diseases.
For the past decade, researchers have been intrigued by the apparent health benefits of resveratrol, which has been shown to fight obesity, type 2 diabetes and cancer in mice and seems to have some health benefits for humans. But no one understood how the chemical worked its magic on the body.
Now a new study from the National Institutes of Health has deciphered just how the chemical interacts with the body’s cells. The research is complicated, but spells out good news for the potential of the red-wine compound to treat chronic diseases.
Dr. Jay Chung, the study’s lead author, said resveratrol is tricky because it’s a “dirty molecule,” meaning it interacts in lots of different ways with the cells of the body, some good and some bad. By first testing cells in the lab and then testing mice, Chung and his team were able to identify which of resveratrol’s cellular hook-ups delivered the chemical’s benefits...
For the past decade, researchers have been intrigued by the apparent health benefits of resveratrol, which has been shown to fight obesity, type 2 diabetes and cancer in mice and seems to have some health benefits for humans. But no one understood how the chemical worked its magic on the body.
Now a new study from the National Institutes of Health has deciphered just how the chemical interacts with the body’s cells. The research is complicated, but spells out good news for the potential of the red-wine compound to treat chronic diseases.
Dr. Jay Chung, the study’s lead author, said resveratrol is tricky because it’s a “dirty molecule,” meaning it interacts in lots of different ways with the cells of the body, some good and some bad. By first testing cells in the lab and then testing mice, Chung and his team were able to identify which of resveratrol’s cellular hook-ups delivered the chemical’s benefits...
Researchers find obesity begins in brain
Though most people think obesity is a problem of hips, thighs and bellies, a new study by US scientists shows that obesity begins in the brain where the female hormone estrogen plays a role.
The study by a group of researchers, led by Baylor College of Medicine and The University of Texas Southwestern Medical School, shows that the hormone works through two populations of neurons, steroidogenic factor-1 (SF-1) neurons and the pro-opiomelanocortin (POMC) neurons, in a particular part of the brain called the hypothalamus.
The researchers found that the two kinds of neurons play different but important roles in metabolism, fat distribution and appetite control, according to the February issue of the Baylor College of Medicine news.
"Before menopause, women are protected from obesity and associated disorders by estrogen," said Dr. Yong Xu, the first author of the study and assistant professor of the USDA Agricultural Research Service Children's Nutrition Research Center at BCM and Texas Children's Hospital.
After menopause, the risk of obesity in women rises, while the risks of estrogen replacement therapy outweigh its effect on reducing obesity, Xu said.
Researchers studied four different kinds of mice to determine the effect of estrogen and focused their work on neurons in the hypothalamus that carry an estrogen receptor alpha. The hypothalamus links the nervous system to the endocrine system to regulate multiple physiological processes, including those controlling bodyweight...
The study by a group of researchers, led by Baylor College of Medicine and The University of Texas Southwestern Medical School, shows that the hormone works through two populations of neurons, steroidogenic factor-1 (SF-1) neurons and the pro-opiomelanocortin (POMC) neurons, in a particular part of the brain called the hypothalamus.
The researchers found that the two kinds of neurons play different but important roles in metabolism, fat distribution and appetite control, according to the February issue of the Baylor College of Medicine news.
"Before menopause, women are protected from obesity and associated disorders by estrogen," said Dr. Yong Xu, the first author of the study and assistant professor of the USDA Agricultural Research Service Children's Nutrition Research Center at BCM and Texas Children's Hospital.
After menopause, the risk of obesity in women rises, while the risks of estrogen replacement therapy outweigh its effect on reducing obesity, Xu said.
Researchers studied four different kinds of mice to determine the effect of estrogen and focused their work on neurons in the hypothalamus that carry an estrogen receptor alpha. The hypothalamus links the nervous system to the endocrine system to regulate multiple physiological processes, including those controlling bodyweight...
Can we ‘catch’ obesity and liver disease? Mice can
Here’s a new study from Yale University that adds another layer of complexity to the obesity puzzle: Lab mice whose intestinal enviroments were altered to create a deficiency in their immune responses developed a population of microbes in their stomachs that led to obesity and liver disease.
And healthy mice, when put in cages with the infected mice, developed the same population of microbes and the same propensity for obesity, metabolic syndrome and chronic liver disease...
And healthy mice, when put in cages with the infected mice, developed the same population of microbes and the same propensity for obesity, metabolic syndrome and chronic liver disease...
Exercise hormone can fight obesity
Irisin, a polypeptide hormone found in both humans and mice is a membrane protein in muscle cells that breaks down during exercise and secreted as a hormone, said researchers at the Dana-Farber Cancer Institute and Harvard Medical School in the US.
The hormone which is named after Iris, the messenger of the gods in Greek mythology acts as a chemical messenger and induces ordinary “white” fat cells to convert into “brown fat,” a type of adipose tissue that helps regulate body temperature, while burning a tremendous amount of energy in the process.
After injecting irisin into mice, researchers found that the hormone switched on genes that convert white fat into “good” brown fat which burns off more excess calories than does exercise alone, says the report published in the journal Nature...
The hormone which is named after Iris, the messenger of the gods in Greek mythology acts as a chemical messenger and induces ordinary “white” fat cells to convert into “brown fat,” a type of adipose tissue that helps regulate body temperature, while burning a tremendous amount of energy in the process.
After injecting irisin into mice, researchers found that the hormone switched on genes that convert white fat into “good” brown fat which burns off more excess calories than does exercise alone, says the report published in the journal Nature...
Could a pill help fight obesity?
Boston researchers have discovered a hormone produced by muscles during exercise which boosts the amount of calories the body burns.
In experiments with mice, Harvard Medical School researchers found that inducing greater levels of the hormone in obese, pre-diabetic mice led to weight loss, increased energy expenditure, and improvements in insulin resistance, which is a risk factor for diabetes...
In experiments with mice, Harvard Medical School researchers found that inducing greater levels of the hormone in obese, pre-diabetic mice led to weight loss, increased energy expenditure, and improvements in insulin resistance, which is a risk factor for diabetes...
Sunday, January 08, 2012
Fatty diet damages brain - study
SCIENTISTS have found a high-fat diet damages a crucial region of the brain that controls body weight in rodents and believe a similar process may occur in obese humans.
Within 24 hours of being fed high-fat foods, rats and mice developed inflammation followed by scarring in the hypothalamus, a region that regulates body weight and food intake in humans and rodents. Animals fed the diet continuously for four weeks developed chronic inflammation and neuron loss.
Within 24 hours of being fed high-fat foods, rats and mice developed inflammation followed by scarring in the hypothalamus, a region that regulates body weight and food intake in humans and rodents. Animals fed the diet continuously for four weeks developed chronic inflammation and neuron loss.
Obesity Linked to Brain Damage
...The notion that brain damage might play a role in body weight is not a new one, according to Michael Schwartz of the Diabetes and Obesity Center at the University of Washington in Seattle.
Scientists have known for about five years that the hypothalamus of overweight animals - including humans - displays inflammation, a typical reaction to injury.
But researchers, led by Schwartz, wanted to determine the role hypothalamus injury plays in obesity, and they had several questions they wanted to answer:
“Is it simply a consequence of becoming obese or does it occur before the obesity occurs?" says Schwartz. "And what could be driving that response? What is causing the inflammatory response and could that have something to do with the obesity itself?”
Schwartz’s team put laboratory mice and rats on a high-fat diet to make them gain weight. When they looked for evidence of inflammation in their brains, they made a startling discovery...
Scientists have known for about five years that the hypothalamus of overweight animals - including humans - displays inflammation, a typical reaction to injury.
But researchers, led by Schwartz, wanted to determine the role hypothalamus injury plays in obesity, and they had several questions they wanted to answer:
“Is it simply a consequence of becoming obese or does it occur before the obesity occurs?" says Schwartz. "And what could be driving that response? What is causing the inflammatory response and could that have something to do with the obesity itself?”
Schwartz’s team put laboratory mice and rats on a high-fat diet to make them gain weight. When they looked for evidence of inflammation in their brains, they made a startling discovery...
Saturday, December 17, 2011
Human enzyme keeps mice slim
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...
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...
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...
Subscribe to:
Posts (Atom)