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’...
Sunday, October 09, 2011
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."...
Sunday, March 06, 2011
Resveratrol can reduce body fat: Study
Resveratrol may be a useful tool for reducing body fat, according to a new study.
For her thesis, Arrate Lasa, nutrition and obesity research team member at the University of the Basque Country, studied the fat-reducing effect of Conjugated Linoleic Acid (CLA) and resveratrol.
CLA and resveratrol are two functional ingredients that, in various experiments on living beings and in vitro, have proved to have a fat-reducing effect.
On the one hand, the properties attributed to CLA indicate that it prevents weight gain and the accumulation of body fat through inhibiting the synthesis of fat and increasing the oxidation of fatty acids.
However, its effects when applied in a hypocaloric diet for the treatment of obesity are unknown.
On the other, it is known that resveratrol has hypolipemiant properties, but its effect on the use of accumulated fat has not been extensively analysed.
Lasa's thesis showed the results obtained after treatment with CLA in hamsters subjected to energy restriction and the effect of resveratrol on accumulated fat and lipolytic activity in cell cultures of adipocytes of murinae and humans.
The results showed that CLA does not foment weight or body fat loss, induced by an energy restriction diet.
Neither does it induce greater lipolysis, nor improvement in serum parametres, in glucose homeostasis or insulin function to any greater extent than with the slimming diet itself.
On the contrary, resveratrol reduces the accumulation of triglycerides, in part by activation of lipolysis, in both the adipocytes of mice and of humans...
For her thesis, Arrate Lasa, nutrition and obesity research team member at the University of the Basque Country, studied the fat-reducing effect of Conjugated Linoleic Acid (CLA) and resveratrol.
CLA and resveratrol are two functional ingredients that, in various experiments on living beings and in vitro, have proved to have a fat-reducing effect.
On the one hand, the properties attributed to CLA indicate that it prevents weight gain and the accumulation of body fat through inhibiting the synthesis of fat and increasing the oxidation of fatty acids.
However, its effects when applied in a hypocaloric diet for the treatment of obesity are unknown.
On the other, it is known that resveratrol has hypolipemiant properties, but its effect on the use of accumulated fat has not been extensively analysed.
Lasa's thesis showed the results obtained after treatment with CLA in hamsters subjected to energy restriction and the effect of resveratrol on accumulated fat and lipolytic activity in cell cultures of adipocytes of murinae and humans.
The results showed that CLA does not foment weight or body fat loss, induced by an energy restriction diet.
Neither does it induce greater lipolysis, nor improvement in serum parametres, in glucose homeostasis or insulin function to any greater extent than with the slimming diet itself.
On the contrary, resveratrol reduces the accumulation of triglycerides, in part by activation of lipolysis, in both the adipocytes of mice and of humans...
Study: Father's diet can influence metabolism of kids
...Working with mice, the researchers reported in the journal Cell that paternal diet can influence the production of genes that direct metabolism in first-generation offspring, and particularly influence how they're able to process cholesterol.
The study is one of a number done recently that look at how the environment and lifestyle of a previous generation can influence the genetics of the next, going beyond traits that are known to be passed from generation to generation through mutations in DNA.
"Knowing what your parents were doing before you were conceived is turning out to be important in determining what disease factors you may be carrying," said Dr. Oliver Rando, an associate professor at the University of Massachusetts and lead investigator for the study.
"Our findings suggest there are many ways that parents can tell their children things."
Rando and his colleagues fed two groups of male mice different diets — one a low-protein diet, the other standard chow; while all the females in the test got the standard diet before breeding started.
They found that the offspring of the male mice fed the low-protein diet showed a marked increase in genes responsible for blood fats and cholesterol breakdown compared to those sired by mice fed the standard diet.
Although the study involved mice, the research actually has its roots in several human observational studies that suggested there was a paternal and even grand-paternal effect from diet on the risks for diabetes, obesity and heart disease...
The study is one of a number done recently that look at how the environment and lifestyle of a previous generation can influence the genetics of the next, going beyond traits that are known to be passed from generation to generation through mutations in DNA.
"Knowing what your parents were doing before you were conceived is turning out to be important in determining what disease factors you may be carrying," said Dr. Oliver Rando, an associate professor at the University of Massachusetts and lead investigator for the study.
"Our findings suggest there are many ways that parents can tell their children things."
Rando and his colleagues fed two groups of male mice different diets — one a low-protein diet, the other standard chow; while all the females in the test got the standard diet before breeding started.
They found that the offspring of the male mice fed the low-protein diet showed a marked increase in genes responsible for blood fats and cholesterol breakdown compared to those sired by mice fed the standard diet.
Although the study involved mice, the research actually has its roots in several human observational studies that suggested there was a paternal and even grand-paternal effect from diet on the risks for diabetes, obesity and heart disease...
Scientists Discover Genetic Switch That Increases Muscle Blood Supply
Many people suffer from a devastating condition known as critical limb ischemia (CLI) that can lead to muscle wasting and even amputation. The disease is linked to the blockage of blood flow to the skeletal muscle and current treatment options include rehabilitative exercise and surgical bypass of blood vessels. New preclinical research suggests there may be a way to restore blood supply in skeletal muscle without traditional intervention.
Scientists at The University of Texas Health Science Center at Houston (UTHealth) and the Salk Institute for Biological Studies announced in the March 2 print issue of the journal Cell Metabolism that they have identified a genetic switch that can increase the number of blood vessels in the skeletal muscle of non-exercising mice.
Skeletal muscle is composed of two types of fibers: slow twitch fibers that inherently have a dense supply of blood vessels and fast twitch fibers that have fewer blood vessels. The researchers used a gene switch known as estrogen-related receptor gamma (ERR gamma) that when activated in fast twitch fibers of mice by genetic engineering, converts these fibers into slow twitch fibers.
"This consequently resulted in a striking increase in muscle blood supply as measured by imaging and angiography," said Vihang Narkar, Ph.D., lead investigator and assistant professor of molecular medicine at the UTHealth Medical School. "These genetically-transformed muscles also acquire other characteristics of slow muscles, such as improved metabolic capacity and fatigue resistance that can be additionally beneficial in resolving muscle vascular disease."
Narkar, whose UTHealth laboratory is in the Center for Diabetes and Obesity Research at the Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases, said, "The identification of the estrogen-related receptor gamma vascular switch will open potential therapeutic avenues for treating CLI and other cardiovascular diseases linked to defective blood supply."
Colin Barker, M.D., assistant professor of cardiology at the UTHealth Medical School, said new research is needed to help people with peripheral artery disease, particularly those with the most severe form - critical limb ischemia. "Poor circulation in the legs can lead to muscle wasting, infections, severe pain, and amputation," he said. "Dr. Narkar's work potentially has many useful applications. It is very much in the translational medicine arena."
"Understanding the gene network that specifies high vascular supply to muscle gives us a new and very powerful tool to promote improved muscle performance and the promise of fitness, especially for those who cannot work out," says Ronald M. Evans, Ph.D., senior author, Howard Hughes Medical Institute Investigator and professor in the Salk Institute's Gene Expression Laboratory. "This is good news for people with heart disease, frailty, peripheral vascular disease, and more generally those who have a variety of medical problems where exercise could be helpful but is not possible to achieve."
In 2010, an estimated 2.8 to 3.5 million U.S. citizens suffered from critical limb ischemia, according to a report by THE SAGE GROUP, an independent research and consulting company specializing in peripheral artery disease. CLI risk factors include diabetes, obesity and smoking...
Scientists at The University of Texas Health Science Center at Houston (UTHealth) and the Salk Institute for Biological Studies announced in the March 2 print issue of the journal Cell Metabolism that they have identified a genetic switch that can increase the number of blood vessels in the skeletal muscle of non-exercising mice.
Skeletal muscle is composed of two types of fibers: slow twitch fibers that inherently have a dense supply of blood vessels and fast twitch fibers that have fewer blood vessels. The researchers used a gene switch known as estrogen-related receptor gamma (ERR gamma) that when activated in fast twitch fibers of mice by genetic engineering, converts these fibers into slow twitch fibers.
"This consequently resulted in a striking increase in muscle blood supply as measured by imaging and angiography," said Vihang Narkar, Ph.D., lead investigator and assistant professor of molecular medicine at the UTHealth Medical School. "These genetically-transformed muscles also acquire other characteristics of slow muscles, such as improved metabolic capacity and fatigue resistance that can be additionally beneficial in resolving muscle vascular disease."
Narkar, whose UTHealth laboratory is in the Center for Diabetes and Obesity Research at the Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases, said, "The identification of the estrogen-related receptor gamma vascular switch will open potential therapeutic avenues for treating CLI and other cardiovascular diseases linked to defective blood supply."
Colin Barker, M.D., assistant professor of cardiology at the UTHealth Medical School, said new research is needed to help people with peripheral artery disease, particularly those with the most severe form - critical limb ischemia. "Poor circulation in the legs can lead to muscle wasting, infections, severe pain, and amputation," he said. "Dr. Narkar's work potentially has many useful applications. It is very much in the translational medicine arena."
"Understanding the gene network that specifies high vascular supply to muscle gives us a new and very powerful tool to promote improved muscle performance and the promise of fitness, especially for those who cannot work out," says Ronald M. Evans, Ph.D., senior author, Howard Hughes Medical Institute Investigator and professor in the Salk Institute's Gene Expression Laboratory. "This is good news for people with heart disease, frailty, peripheral vascular disease, and more generally those who have a variety of medical problems where exercise could be helpful but is not possible to achieve."
In 2010, an estimated 2.8 to 3.5 million U.S. citizens suffered from critical limb ischemia, according to a report by THE SAGE GROUP, an independent research and consulting company specializing in peripheral artery disease. CLI risk factors include diabetes, obesity and smoking...
Sunday, February 27, 2011
Diet and exercise restore immune function in obesity
Boston University scientists say that moderate daily exercise and dietary control might reverse immune dysfunctions found in people with obesity.
Overeating and a sedentary lifestyle are well-known risk factors for obesity, which is linked to hypertension, heart disease, diabetes, gum disease, certain cancers, and asthma.
Research has suggested that a change in immune function is a predecessor to all these diseases and researchers at Boston University Henry M. Goldman School of Dental Medicine (GSDM) have previously shown that obesity causes immune defects that make it hard to fight infection.
Until now, little was known about how diet and exercise affects immunity in obese people.
Researchers worked with diet-induced obese mice in four groups:
• lean mice on a standard chow diet
• obese mice on a high fat diet
• obese mice on a high fat diet on a moderate exercise plan for four weeks, and
• obese, high fat diet mice given moderate exercise and a four-week standard chow diet
Moderate daily exercise and dietary control dramatically restored immune function. Obese mice saw damaged cytokines—signaling molecules that help immune cells talk to each other—repaired and an improved ability to fight gum disease as measured by bone loss.
“The study underscores the necessity to correct two important factors in obesity—diet and exercise—to improve markers of immune dysfunction and bone loss,” says senior author Dr. Salomon Amar. “The correction of one factor only may not lead to any tangible changes.”...
Overeating and a sedentary lifestyle are well-known risk factors for obesity, which is linked to hypertension, heart disease, diabetes, gum disease, certain cancers, and asthma.
Research has suggested that a change in immune function is a predecessor to all these diseases and researchers at Boston University Henry M. Goldman School of Dental Medicine (GSDM) have previously shown that obesity causes immune defects that make it hard to fight infection.
Until now, little was known about how diet and exercise affects immunity in obese people.
Researchers worked with diet-induced obese mice in four groups:
• lean mice on a standard chow diet
• obese mice on a high fat diet
• obese mice on a high fat diet on a moderate exercise plan for four weeks, and
• obese, high fat diet mice given moderate exercise and a four-week standard chow diet
Moderate daily exercise and dietary control dramatically restored immune function. Obese mice saw damaged cytokines—signaling molecules that help immune cells talk to each other—repaired and an improved ability to fight gum disease as measured by bone loss.
“The study underscores the necessity to correct two important factors in obesity—diet and exercise—to improve markers of immune dysfunction and bone loss,” says senior author Dr. Salomon Amar. “The correction of one factor only may not lead to any tangible changes.”...
Treadmill the fountain of youth: study
Exercising on a treadmill for 45 minutes, three times a week, warded off the effects of premature aging in lab mice, a McMaster University study shows.
The researchers hope that when people see the dramatic difference between sedentary mice and those with the treadmill routine, it’ll give them an extra push to get off the couch.
Anything that motivates people to exercise is beneficial because it’s good for human health, decreasing rates of obesity and Type 2 diabetes while increasing longevity, said Dr. Mark Tarnopolsky of McMaster’s Michael G. DeGroote School of Medicine...
The researchers hope that when people see the dramatic difference between sedentary mice and those with the treadmill routine, it’ll give them an extra push to get off the couch.
Anything that motivates people to exercise is beneficial because it’s good for human health, decreasing rates of obesity and Type 2 diabetes while increasing longevity, said Dr. Mark Tarnopolsky of McMaster’s Michael G. DeGroote School of Medicine...
New research suggests that obesity and diabetes are a downside of human evolution
...In this study, which is the first to examine the effect of a human-specific CMAH genetic mutation in obesity-related metabolism and diabetes, Kim and colleagues show that the loss of CMAH's function contributes to the failure of the insulin-producing pancreatic beta cells in overweight humans, which is known to be a key factor in the development of type 2 diabetes. This gene encodes for an enzyme present in all mammalian species except for humans and adds a single oxygen atom to sialic acids, which are sugars that coat the cell surface.
To make their discovery, the researchers used two groups of mice. The first group had the same mutant CMAH gene found in humans. These mice demonstrated that the CMAH enzyme was inactive and could not produce a sialic acid type called NeuSGc at the cell surface. The second group had a normal CMAH gene. When exposed to a high fat diet, both sets of mice developed insulin resistance as a result of their obesity. Pancreatic beta cell failure, however, occurred only in the CMAH mutant mice that lacked NeuSGc, resulting in a decreased insulin production, which then further impaired blood glucose level control. This discovery may enhance scientific understanding of why humans may be particularly prone to develop type 2 diabetes. Results may also suggest that conventional animal models may not accurately mirror the human situation.
"The diabetes discovery is an important advance in its own right. It tells us a lot about what goes wrong in diabetes, and where to aim with new treatments," said Gerald Weissmann, M.D., Editor-in-Chief of the FASEB Journal, "but its implications for human evolution are even greater. If this enzyme is unique to humans, it must also have given us a survival advantage over earlier species. Now the challenge is to find the function of CMAH in defending us against microbes or environmental stress or both. This evolutionary science explains how we can win some and lose some, to keep our species ahead of the extinction curve."
To make their discovery, the researchers used two groups of mice. The first group had the same mutant CMAH gene found in humans. These mice demonstrated that the CMAH enzyme was inactive and could not produce a sialic acid type called NeuSGc at the cell surface. The second group had a normal CMAH gene. When exposed to a high fat diet, both sets of mice developed insulin resistance as a result of their obesity. Pancreatic beta cell failure, however, occurred only in the CMAH mutant mice that lacked NeuSGc, resulting in a decreased insulin production, which then further impaired blood glucose level control. This discovery may enhance scientific understanding of why humans may be particularly prone to develop type 2 diabetes. Results may also suggest that conventional animal models may not accurately mirror the human situation.
"The diabetes discovery is an important advance in its own right. It tells us a lot about what goes wrong in diabetes, and where to aim with new treatments," said Gerald Weissmann, M.D., Editor-in-Chief of the FASEB Journal, "but its implications for human evolution are even greater. If this enzyme is unique to humans, it must also have given us a survival advantage over earlier species. Now the challenge is to find the function of CMAH in defending us against microbes or environmental stress or both. This evolutionary science explains how we can win some and lose some, to keep our species ahead of the extinction curve."
Monday, February 14, 2011
Mapping obesity circuitry in brain
In the battle of the bulge, one important battalion is a set of brain cells expressing the melanocortin-4 receptor (MC4R). Via signals from the fat-derived hormone leptin, these neurons regulate feeding behavior and fat metabolism in an attempt to regulate body weight. But how leptin influences and acts on this brain circuitry is not fully understood.
Using mice with fluorescently-tagged MC4R, Masoud Ghamari-Langroudi, Roger Cone and colleagues analyzed how the activity of MC4R neurons of the paraventricular nucleus of the hypothalamus (PVN) are regulated by leptin and by metabolic state (i.e., fasting).
They report in the Jan. 4 Proceedings of the National Academy of Sciences that fasting increases firing of these neurons and that leptin administration returns the firing to normal levels. They also show that contrary to the conventional view that leptin indirectly regulates PVN neuron activity, it can also inhibit the activity of PVN neurons directly. Such details of the brain circuitry underlying energy balance could provide important clues to understanding – and combating – obesity.
Using mice with fluorescently-tagged MC4R, Masoud Ghamari-Langroudi, Roger Cone and colleagues analyzed how the activity of MC4R neurons of the paraventricular nucleus of the hypothalamus (PVN) are regulated by leptin and by metabolic state (i.e., fasting).
They report in the Jan. 4 Proceedings of the National Academy of Sciences that fasting increases firing of these neurons and that leptin administration returns the firing to normal levels. They also show that contrary to the conventional view that leptin indirectly regulates PVN neuron activity, it can also inhibit the activity of PVN neurons directly. Such details of the brain circuitry underlying energy balance could provide important clues to understanding – and combating – obesity.
Diet drug makers seeking new strategies
...The search for new drug pathways that alter the body’s metabolism, and the way calories are burned and stored as fat, gained momentum in 2009 when researchers from the University of Michigan, Vanderbilt University and Fudan University in Shanghai published a paper in the journal Cell exploring the relationship between inflammation in the fat tissue of mice and obesity and diabetes.
They focused on a protein that activates immune-system white blood cells that cause fat cells to swell.
In regular mice that were fed a high-calorie diet, the protein activated white blood cells, causing fat cells to swell. The mice gained weight and became insulin-resistant, a condition known as Type 2 diabetes.
Another group of mice were genetically engineered to lack the protein. Those animals were also overfed, but they didn’t gain weight. Instead, their bodies consumed more oxygen and produced greater amounts of another type of protein that generates body heat by burning fat tissue.
As an added benefit, the engineered mice didn’t develop diabetes.
They focused on a protein that activates immune-system white blood cells that cause fat cells to swell.
In regular mice that were fed a high-calorie diet, the protein activated white blood cells, causing fat cells to swell. The mice gained weight and became insulin-resistant, a condition known as Type 2 diabetes.
Another group of mice were genetically engineered to lack the protein. Those animals were also overfed, but they didn’t gain weight. Instead, their bodies consumed more oxygen and produced greater amounts of another type of protein that generates body heat by burning fat tissue.
As an added benefit, the engineered mice didn’t develop diabetes.
Mayo Clinic researcher's memory study leads to surprising obesity finding
Their mission was to solve a small but nagging mystery of Alzheimer's disease: How would the brain's ability to store information be affected if they "turned off" the obscure protein LRP1?
But Guojun Bu and his fellow researchers were in for a surprise. As they expected, mice whose brains had been wiped of the LRP1 gene showed Alzheimer's-like memory problems. But they also started to put on weight - fast.
The mice were lethargic. They were on their way to becoming diabetic. And they didn't seem to know when to stop eating.
In other words, they were a lot like the more than 72 million Americans who are obese...
But Guojun Bu and his fellow researchers were in for a surprise. As they expected, mice whose brains had been wiped of the LRP1 gene showed Alzheimer's-like memory problems. But they also started to put on weight - fast.
The mice were lethargic. They were on their way to becoming diabetic. And they didn't seem to know when to stop eating.
In other words, they were a lot like the more than 72 million Americans who are obese...
Sunday, February 06, 2011
Obesity resistant mechanisms in the Lean polygenic mouse model as indicated by liver transcriptome and expression of selected genes in skeletal muscle
Divergently selected Lean and Fat mouse lines represent unique models for a polygenic form of resistance and susceptibility to obesity development. Previous research on these lines focused mainly on obesity-susceptible factors in the Fat line.
This study aimed to examine the molecular basis of obesity-resistant mechanisms in the Lean line by analyzing various fat depots and organs, the liver transcriptome of selected metabolic pathways, plasma and lipid homeostasis and expression of selected skeletal muscle genes.
Results: Expression profiling using our custom Steroltalk v2 microarray demonstrated that Lean mice exhibit a higher hepatic expression of cholesterol biosynthesis genes compared to the Fat line...
This study aimed to examine the molecular basis of obesity-resistant mechanisms in the Lean line by analyzing various fat depots and organs, the liver transcriptome of selected metabolic pathways, plasma and lipid homeostasis and expression of selected skeletal muscle genes.
Results: Expression profiling using our custom Steroltalk v2 microarray demonstrated that Lean mice exhibit a higher hepatic expression of cholesterol biosynthesis genes compared to the Fat line...
Biochemistry analyses mouse resistance to obesity
Mechanisms that allow mice to resist developing obesity have been analysed using gel filtration chromatography by a team of French and Slovenian biochemistry and veterinary scientists...
Sunday, January 30, 2011
New molecular player responsible for regulation of appetite and metabolism
A study by researchers at Mayo Clinic's campus in Florida and Washington University School of Medicine adds a new twist to the body of evidence suggesting human obesity is due in part to genetic factors. While studying hormone receptors in laboratory mice, neuroscientists identified a new molecular player responsible for the regulation of appetite and metabolism...
Study suggests designer probiotics could help cut obesity
Targeted probiotics could affect the physiology of human fat cells and potentially prevent or help treat conditions such as obesity, according to new Irish research.
Recently published in Microbiology, the study from scientists at Teagasc (the Irish Agriculture and Food Development Authority), University College Cork and the Alimentary Pharmabiotic Centre examined whether a lactobacillus strain with CLA (conjugated linoleic acid) influenced fat tissue composition in mice.
Previous research from Racine et al. (2010) and Thom et al. (2001) has linked fatty acid t10, c12 CLA consumption with decreased body fat in humans, while other studies suggest that this type of fatty acid inhibits colon cancer cell growth.
Probiotics assists CLA metabolism
In this study, scientists transferred an enzyme-encoding gene from skin bacterium P.acnes to Lactobacillus paracasei and induced it to produce CLA t10, c12, which fed to mice resulted in a fourfold increase of CLA in mouse fat tissue composition (against a second probiotic control strain) showing that live bacteria intake affects metabolism at remote body sites...
Warmer Houses May Increase Obesity
...Unlike mice fed a typical low-fat laboratory diet, adjusting their intake to the ambient temperature, mice fed high-fat diets do not decrease their food intake at higher temperatures and gain weight.
"These human and animal experimental models suggest that while intake is somewhat suppressed at higher temperatures, this is unlikely to fully compensate for the reduced energy expenditure of a warm environment particularly where highly palatable foods are available," Johnson and colleagues observed.
This research argues in favor of a causal link between increased time spent in thermal comfort and weight gain in the population, they said...
"These human and animal experimental models suggest that while intake is somewhat suppressed at higher temperatures, this is unlikely to fully compensate for the reduced energy expenditure of a warm environment particularly where highly palatable foods are available," Johnson and colleagues observed.
This research argues in favor of a causal link between increased time spent in thermal comfort and weight gain in the population, they said...
Obesity Drug Moving to Clinical Trials Following Success in Mice, Dogs, and Women
A successful trial on a small number of obese women in Australia demonstrated that those treated with intravenous Zafgen-433 lost an average of approximately two pounds per week. In addition to the weight loss, the women experienced a decline in hunger and reductions in triglycerides and low-density lipoprotein (LDL) cholesterol levels, all with no serious, treatment-related adverse events. Now, following the positive results of this initial double-blind, placebo-controlled, proof-of-concept trial, Zafgen expects to have a subcutaneous form of the drug ready by the end of summer which will be used for the next phase of clinical trials (for both men and women) expected to begin sometime later in 2011. Ultimately, though, the company plans to create a conventional, oral form of the medication...
Zafgen's innovative approach to reversing obesity targets adipose tissue (fat cells) because, unlike the traditional view of obesity that fat accumulation is a "passive result of other factors," Zafgen views adipose tissue "as playing an active role in the disease," a view that represents a "fundamentally new paradigm" in how obesity is regarded and potentially treated. Indeed, obese people release fat from their adipose tissue at a slower rate than the non-obese, and they convert it to ketone bodies – a form that is usable as fuel for muscles – at a slower rate. (Much of this process encompasses the metabolic syndrome and insulin resistance that doctors described when discussing obesity as a risk for type 2 diabetes.) Zafgen-433 acts on adipose tissue by inhibiting an enzyme called methionine aminopeptidase 2, or MetAP2, an enzyme that is associated with the body's tendency for preserving its stores of fat. When this enzyme is inhibited by the drug, it allows the body to metabolize fatty acids at a more normalized rate as the body re-establishes its balance, leading to a substantial loss of body weight in overweight individuals. This was true for the overfed mice (pictured above), for overweight dogs, and for the initial trial of obese women in Australia. Adipose tissue samples from the treated mice revealed that their fat cells actually shrank...
Zafgen's innovative approach to reversing obesity targets adipose tissue (fat cells) because, unlike the traditional view of obesity that fat accumulation is a "passive result of other factors," Zafgen views adipose tissue "as playing an active role in the disease," a view that represents a "fundamentally new paradigm" in how obesity is regarded and potentially treated. Indeed, obese people release fat from their adipose tissue at a slower rate than the non-obese, and they convert it to ketone bodies – a form that is usable as fuel for muscles – at a slower rate. (Much of this process encompasses the metabolic syndrome and insulin resistance that doctors described when discussing obesity as a risk for type 2 diabetes.) Zafgen-433 acts on adipose tissue by inhibiting an enzyme called methionine aminopeptidase 2, or MetAP2, an enzyme that is associated with the body's tendency for preserving its stores of fat. When this enzyme is inhibited by the drug, it allows the body to metabolize fatty acids at a more normalized rate as the body re-establishes its balance, leading to a substantial loss of body weight in overweight individuals. This was true for the overfed mice (pictured above), for overweight dogs, and for the initial trial of obese women in Australia. Adipose tissue samples from the treated mice revealed that their fat cells actually shrank...
Sunday, January 23, 2011
Effects of diet-induced obesity and voluntary wheel running on the microstructure of the murine distal femur
Backgound: Obesity and osteoporosis, two possibly related conditions, are rapidly expanding health concerns in modern society. Both of them are associated with sedentary life style and nutrition.
To investigate the effects of diet-induced obesity and voluntary physical activity we used high resolution micro-computed tomography (uCT) together with peripheral quantitative computed tomography (pQCT) to examine the microstructure of the distal femoral metaphysis in mice.
Methods: Forty 7-week-old male C57BL/6J mice were assigned to 4 groups: control (C), control + running (CR), high-fat diet (HF), and high-fat diet + running (HFR). After a 21-week intervention, all the mice were sacrificed and the left femur dissected for pQCT and uCT measurements.
Results: The mice fed the high-fat diet showed a significant weight gain (over 70% for HF and 60% for HFR), with increased epididymal fat pad mass and impaired insulin sensitivity.
These obese mice had significantly higher trabecular connectivity density, volume, number, thickness, area and mass, and smaller trabecular separation. At the whole bone level, they had larger bone circumference and cross-sectional area and higher density-weighted maximal, minimal, and polar moments of inertia.
Voluntary wheel running decreased all the cortical bone parameters, but increased the trabecular mineral density, and decreased the pattern factor and structure model index towards a more plate-like structure.
Conclusions: The results suggest that in mice the femur adapts to obesity by improving bone strength both at the whole bone and micro-structural level. Adaptation to running exercise manifests itself in increased trabecular density and improved 3D structure, but in a limited overall bone growth...
To investigate the effects of diet-induced obesity and voluntary physical activity we used high resolution micro-computed tomography (uCT) together with peripheral quantitative computed tomography (pQCT) to examine the microstructure of the distal femoral metaphysis in mice.
Methods: Forty 7-week-old male C57BL/6J mice were assigned to 4 groups: control (C), control + running (CR), high-fat diet (HF), and high-fat diet + running (HFR). After a 21-week intervention, all the mice were sacrificed and the left femur dissected for pQCT and uCT measurements.
Results: The mice fed the high-fat diet showed a significant weight gain (over 70% for HF and 60% for HFR), with increased epididymal fat pad mass and impaired insulin sensitivity.
These obese mice had significantly higher trabecular connectivity density, volume, number, thickness, area and mass, and smaller trabecular separation. At the whole bone level, they had larger bone circumference and cross-sectional area and higher density-weighted maximal, minimal, and polar moments of inertia.
Voluntary wheel running decreased all the cortical bone parameters, but increased the trabecular mineral density, and decreased the pattern factor and structure model index towards a more plate-like structure.
Conclusions: The results suggest that in mice the femur adapts to obesity by improving bone strength both at the whole bone and micro-structural level. Adaptation to running exercise manifests itself in increased trabecular density and improved 3D structure, but in a limited overall bone growth...
The Microbes In Our Gut Regulate Genes That Control Obesity And Inflammation
If you are looking to lose weight in the coming year, you may need help from an unexpected place: the bacteria in your gut. That's because scientists have discovered that the bacteria living in your intestines may play a far more significant role in weight loss and gastrointestinal problems than ever imagined. In a new research report published online in The FASEB Journal (http://www.fasebj.org), researchers show that a deficiency of Toll-like receptor 2 (Tlr2) - used by mammals (including humans) to recognize resident microbes in the intestines - leads to changes in gut bacteria that resemble those of lean animals and humans. This discovery builds on previous research demonstrating that a deficiency of TLR2 protects against obesity, while at the same time promoting gastrointestinal problems like excessive inflammation. It also shows that genes controlling TLR2 expression play a very important role in one's gastrointestinal health and weight management.
"Our work highlights the remarkable capacity for an orchestrated reprogramming of the intestinal inflammatory network to overcome significant genetic challenges in the mammalian bowel," said Richard Kellermayer, Ph.D., a researcher involved in the work from the Section of Pediatric Gastroenterology, Hepatology and Nutrition at Baylor College of Medicine in Houston. "The appropriate exploitation of this remarkable capacity may provide means for the prevention and optimized treatment of common metabolic (such as obesity and diabetes) and gastrointestinal disorders."
To make this discovery, Kellermayer and colleagues studied normal mice and mice deficient in TLR2 using the large intestinal lining of these mice. They compared the TLR2-deficient ones to the normal group, as well as the bacteria, the epigenome (more specifically DNA methylation, a molecular change in the DNA associated with decreased gene expression), and the gene expression of the animals. The researchers found that the absence of TLR2 leads to microbial changes in the gut that resemble lean animals and humans, as well as immunologic changes similar to those observed in ulcerative colitis...
"Our work highlights the remarkable capacity for an orchestrated reprogramming of the intestinal inflammatory network to overcome significant genetic challenges in the mammalian bowel," said Richard Kellermayer, Ph.D., a researcher involved in the work from the Section of Pediatric Gastroenterology, Hepatology and Nutrition at Baylor College of Medicine in Houston. "The appropriate exploitation of this remarkable capacity may provide means for the prevention and optimized treatment of common metabolic (such as obesity and diabetes) and gastrointestinal disorders."
To make this discovery, Kellermayer and colleagues studied normal mice and mice deficient in TLR2 using the large intestinal lining of these mice. They compared the TLR2-deficient ones to the normal group, as well as the bacteria, the epigenome (more specifically DNA methylation, a molecular change in the DNA associated with decreased gene expression), and the gene expression of the animals. The researchers found that the absence of TLR2 leads to microbial changes in the gut that resemble lean animals and humans, as well as immunologic changes similar to those observed in ulcerative colitis...
Sunday, January 16, 2011
A magic calorie ride
Bob, an office supervisor in Toronto, considers himself an addict. But the substance he’s prone to abusing isn’t drugs or alcohol—it’s food. “I would gorge on Raisinets, pizza, anything that I could get in quantity,” says Bob, 60, who asked that his last name not be used. He ran up a $4,000 Visa bill, almost all of it on food. Eating as a stress release, “I averaged about 15,000 calories a day.” He weighed 336 lb. at his heaviest. “I’m no scientist, but I think it’s an addiction,” he says. “When I read about how a drug addict behaves, my response is the same to food.”
The term “food addiction” is controversial, but recent studies have shown that high-calorie foods engage the same regions of the brain as drugs like heroin and cocaine. Over time, scientists say, a high-fat diet can impair the brain’s pleasure centres like those drugs do, encouraging ever-larger binges and making it harder to quit. Remarkably, a mother’s diet might even hard-wire her baby for obesity later on in life. “It’s too early to call it food addiction,” says Teresa Reyes of the University of Pennsylvania School of Medicine, who studies how the brain adapts to changes in diet. “But there is absolutely increasing evidence showing that the brain responds to high-sucrose, high-fat diets in a very similar way that it responds to drugs of abuse.”
At the Society for Neuroscience’s annual conference in November, Reyes presented her latest work: mice that were fed a high-fat diet for a long period of time, she found, showed changes in parts of their brains associated with pleasure and reward. Just like cocaine or heroin, unhealthy foods seem to trigger the brain’s pleasure centres, eventually desensitizing them. It becomes a vicious cycle. “To reach the same level of reward, the person needs to eat more rewarding food,” Reyes says. “It’s very similar to what happens in chronic drug abuse.” (This data is now under review before publication.)...
The term “food addiction” is controversial, but recent studies have shown that high-calorie foods engage the same regions of the brain as drugs like heroin and cocaine. Over time, scientists say, a high-fat diet can impair the brain’s pleasure centres like those drugs do, encouraging ever-larger binges and making it harder to quit. Remarkably, a mother’s diet might even hard-wire her baby for obesity later on in life. “It’s too early to call it food addiction,” says Teresa Reyes of the University of Pennsylvania School of Medicine, who studies how the brain adapts to changes in diet. “But there is absolutely increasing evidence showing that the brain responds to high-sucrose, high-fat diets in a very similar way that it responds to drugs of abuse.”
At the Society for Neuroscience’s annual conference in November, Reyes presented her latest work: mice that were fed a high-fat diet for a long period of time, she found, showed changes in parts of their brains associated with pleasure and reward. Just like cocaine or heroin, unhealthy foods seem to trigger the brain’s pleasure centres, eventually desensitizing them. It becomes a vicious cycle. “To reach the same level of reward, the person needs to eat more rewarding food,” Reyes says. “It’s very similar to what happens in chronic drug abuse.” (This data is now under review before publication.)...
Bacteria in the gut help control obesity and inflammation
Researchers at Baylor College of Medicine in Houston have discovered that the bacteria living in the intestines may play a far more significant role in weight loss and gastrointestinal problems than ever imagined.
They show that a deficiency of Toll-like receptor 2 (Tlr2)-used by mammals (including humans) to recognize resident microbes in the intestines-leads to changes in gut bacteria that resemble those of lean animals and humans.
This discovery builds on previous research demonstrating that a deficiency of TLR2 protects against obesity, while at the same time promoting gastrointestinal problems like excessive inflammation.
It also shows that genes controlling TLR2 expression play a very important role in one's gastrointestinal health and weight management.
The team studied normal mice and mice deficient in TLR2 using the large intestinal lining of these mice. They compared the TLR2-deficient ones to the normal group, as well as the bacteria, the epigenome and the gene expression of the animals.
The researchers found that the absence of TLR2 leads to microbial changes in the gut that resemble lean animals and humans, as well as immunologic changes similar to those observed in ulcerative colitis...
They show that a deficiency of Toll-like receptor 2 (Tlr2)-used by mammals (including humans) to recognize resident microbes in the intestines-leads to changes in gut bacteria that resemble those of lean animals and humans.
This discovery builds on previous research demonstrating that a deficiency of TLR2 protects against obesity, while at the same time promoting gastrointestinal problems like excessive inflammation.
It also shows that genes controlling TLR2 expression play a very important role in one's gastrointestinal health and weight management.
The team studied normal mice and mice deficient in TLR2 using the large intestinal lining of these mice. They compared the TLR2-deficient ones to the normal group, as well as the bacteria, the epigenome and the gene expression of the animals.
The researchers found that the absence of TLR2 leads to microbial changes in the gut that resemble lean animals and humans, as well as immunologic changes similar to those observed in ulcerative colitis...
New findings may lead to a novel treatment for obesity
Scientists have added a new twist to the body of evidence suggesting human obesity is due in part to genetic factors.
While studying hormone receptors in laboratory mice, researchers at Mayo Clinic's campus in Florida and Washington University School of Medicine identified a new molecular player responsible for the regulation of appetite and metabolism.
The authors report that mice engineered not to express the lipoprotein receptor LRP1, in the brain's hypothalamus, began to eat uncontrollably, growing obese as well as lethargic. They found that LRP1, a major transporter of lipids and proteins into brain cells, is a "co-receptor" with the leptin receptor - meaning that both the leptin and LRP1 receptors need to work together to transmit leptin signals.
Leptin decides whether fat should be stored or used, resulting in lethargy or energy. When working properly, the hormone, which is made when body cells take in fat from food, travels to the brain to tamp down appetite...
While studying hormone receptors in laboratory mice, researchers at Mayo Clinic's campus in Florida and Washington University School of Medicine identified a new molecular player responsible for the regulation of appetite and metabolism.
The authors report that mice engineered not to express the lipoprotein receptor LRP1, in the brain's hypothalamus, began to eat uncontrollably, growing obese as well as lethargic. They found that LRP1, a major transporter of lipids and proteins into brain cells, is a "co-receptor" with the leptin receptor - meaning that both the leptin and LRP1 receptors need to work together to transmit leptin signals.
Leptin decides whether fat should be stored or used, resulting in lethargy or energy. When working properly, the hormone, which is made when body cells take in fat from food, travels to the brain to tamp down appetite...
Sunday, January 09, 2011
Thanks, Dad
Fathers, as well as mothers, can pass on a propensity to obesity if they themselves have been starved
THAT a gestating mother’s environment can have a permanent effect on the physiology of her offspring is well established. The children of Dutch women who were pregnant during the “Hunger Winter” of 1944, for example, suffer much higher rates of obesity, diabetes and cardiovascular disease than those born a year or two earlier. Similar observations in other famines, together with experiments on rodents, suggest this is an accidental consequence of an evolutionary adaptation to food scarcity. The offspring of starving mothers, anticipating hard times during their own future lives, adjust their metabolisms to hoard calories. If the hard times then go away, the result is a tendency to put on weight, with the unpleasant consequences that entails.
Part of this adaptation is a response by the embryo to the nutrition it receives through the placenta. In some cases, though, the unfertilised ovum itself is believed to be affected. Its DNA is reprogrammed, the theory goes, by a process called cytosine methylation. This switches genes on and off in a way that is maintained when DNA replicates during the process of cell division—and can thus be passed down the generations. It is, moreover, a process that could apply equally to the sperm of putative fathers who were starved around the time of mating.
There are hints that it does. In particular, a recent paper by Sheau-Fang Ng of the University of New South Wales showed that gene activity in the pancreases of mice sired by fat fathers is abnormal. That is significant because the pancreas makes insulin, which regulates blood sugar. Abnormal insulin levels cause diabetes...
THAT a gestating mother’s environment can have a permanent effect on the physiology of her offspring is well established. The children of Dutch women who were pregnant during the “Hunger Winter” of 1944, for example, suffer much higher rates of obesity, diabetes and cardiovascular disease than those born a year or two earlier. Similar observations in other famines, together with experiments on rodents, suggest this is an accidental consequence of an evolutionary adaptation to food scarcity. The offspring of starving mothers, anticipating hard times during their own future lives, adjust their metabolisms to hoard calories. If the hard times then go away, the result is a tendency to put on weight, with the unpleasant consequences that entails.
Part of this adaptation is a response by the embryo to the nutrition it receives through the placenta. In some cases, though, the unfertilised ovum itself is believed to be affected. Its DNA is reprogrammed, the theory goes, by a process called cytosine methylation. This switches genes on and off in a way that is maintained when DNA replicates during the process of cell division—and can thus be passed down the generations. It is, moreover, a process that could apply equally to the sperm of putative fathers who were starved around the time of mating.
There are hints that it does. In particular, a recent paper by Sheau-Fang Ng of the University of New South Wales showed that gene activity in the pancreases of mice sired by fat fathers is abnormal. That is significant because the pancreas makes insulin, which regulates blood sugar. Abnormal insulin levels cause diabetes...
Why are men getting so chubby?
British men are getting fatter than ever, faster than ever. Last week, Oxford University –scientists reported that the average man is more than a stone heavier — 17lb — than 20 years ago.
It would be easy to blame this dramatic increase on over-eating and lack of exercise, and leave it that. But the Oxford study showed that the explanation isn’t this simple.
Indeed, scientific research is revealing that a cocktail of unexpected factors is helping to drive the male obesity epidemic. These include genetics, pollution, stress, vanity, insomnia —and flabby friends.
A bigger Bond: Pierce Brosnan has piled on the pounds since playing the famous spy, right, in Die Another Day
There’s no doubt that British men are eating more. Over their 14-year study period, the Oxford researchers found that around 10.4lb of the extra weight men are carrying was due to extra calories.
But that did not explain the full 17?lb rise. And lack of exercise could only partly account for the difference, says the study leader, Dr Peter Scarborough.
By contrast, the extra 12lb the average woman gained over the same time is entirely explained by them eating more, according to the study, which was published in the British Journal of Nutrition.
This tallies with official statistics that show that nearly half of British men are overweight, compared with just a third of women, while a quarter of men are officially obese (compared with only 7 per cent in 1987).
The result is an epidemic of obesity-related diseases in men: cases of –diabetes have risen by almost a third since 2003, while in women they rose by less than a quarter. Overweight men also have much higher rates of cancer, stroke and heart disease.
More...
Confidence crisis: How the average overweight woman feels humiliated on a daily basis
How most size 12 women still believe they are too fat
Love yourself slim! Want to lose weight? The secret is to think you’re beautiful just the way you are right now
But if overeating and under-exercising are not solely to blame for men’s obesity and disease, what else might be making them fatter?
Research in this field is in its infancy compared with studies of women, but it indicates men have a unique –propensity to put on weight. In November, for example, U.S. –scientists reported they’d found a gene that causes weight gain in men, but not women.
The gene — Arrdc3 — is found in human fat and muscle, but seems to cause only men to become fat as they get older, says lead researcher Dr Parth Patwari of Brigham and Women’s Hospital in Massachusetts.
When he removed the gene from male mice, they no longer suffered from age-related weight gain; in fact, they showed a ‘striking –resistance’ to it. But when the gene was removed from female mice, it made no significant difference...
It would be easy to blame this dramatic increase on over-eating and lack of exercise, and leave it that. But the Oxford study showed that the explanation isn’t this simple.
Indeed, scientific research is revealing that a cocktail of unexpected factors is helping to drive the male obesity epidemic. These include genetics, pollution, stress, vanity, insomnia —and flabby friends.
A bigger Bond: Pierce Brosnan has piled on the pounds since playing the famous spy, right, in Die Another Day
There’s no doubt that British men are eating more. Over their 14-year study period, the Oxford researchers found that around 10.4lb of the extra weight men are carrying was due to extra calories.
But that did not explain the full 17?lb rise. And lack of exercise could only partly account for the difference, says the study leader, Dr Peter Scarborough.
By contrast, the extra 12lb the average woman gained over the same time is entirely explained by them eating more, according to the study, which was published in the British Journal of Nutrition.
This tallies with official statistics that show that nearly half of British men are overweight, compared with just a third of women, while a quarter of men are officially obese (compared with only 7 per cent in 1987).
The result is an epidemic of obesity-related diseases in men: cases of –diabetes have risen by almost a third since 2003, while in women they rose by less than a quarter. Overweight men also have much higher rates of cancer, stroke and heart disease.
More...
Confidence crisis: How the average overweight woman feels humiliated on a daily basis
How most size 12 women still believe they are too fat
Love yourself slim! Want to lose weight? The secret is to think you’re beautiful just the way you are right now
But if overeating and under-exercising are not solely to blame for men’s obesity and disease, what else might be making them fatter?
Research in this field is in its infancy compared with studies of women, but it indicates men have a unique –propensity to put on weight. In November, for example, U.S. –scientists reported they’d found a gene that causes weight gain in men, but not women.
The gene — Arrdc3 — is found in human fat and muscle, but seems to cause only men to become fat as they get older, says lead researcher Dr Parth Patwari of Brigham and Women’s Hospital in Massachusetts.
When he removed the gene from male mice, they no longer suffered from age-related weight gain; in fact, they showed a ‘striking –resistance’ to it. But when the gene was removed from female mice, it made no significant difference...
How the brain's use of fatty acids is linked to obesity
Researchers have established a link between how lipid sensing and metabolism in the brain relate to the regulation of energy balance and body weight.
Hong Wang of University of Colorado created mice with a deficiency of lipoprotein lipase (LPL) in neurons, and observed that the mouse models ate less and they became sedentary.
"This work may have important impact in understanding the causes of obesity and providing new treatments for this epidemic of our time," said Robert H. Eckel.
These mice became obese on a standard chow diet between three and six months. The research also looked at which areas of the brain have the greatest impact on regulating body weight...
Hong Wang of University of Colorado created mice with a deficiency of lipoprotein lipase (LPL) in neurons, and observed that the mouse models ate less and they became sedentary.
"This work may have important impact in understanding the causes of obesity and providing new treatments for this epidemic of our time," said Robert H. Eckel.
These mice became obese on a standard chow diet between three and six months. The research also looked at which areas of the brain have the greatest impact on regulating body weight...
Tree Bark Drug To Fight Obesity
A new drug which contains an element found in the bark of trees may be able to provide new treatments for obesity as well as a number of other major illnesses. The compound, Betulin, which is found in abundance in the bark of birch trees, is able to target genes that produce fats in the blood stream.
In trials it has helped to prevent obesity induced by dietary factors as well as reducing the risk of both diabetes and heart disease. Mice that were fed an atypical high-fat diet when then treated with betulin. The compound caused the mice led to increase the rate at which they burned calories...
In trials it has helped to prevent obesity induced by dietary factors as well as reducing the risk of both diabetes and heart disease. Mice that were fed an atypical high-fat diet when then treated with betulin. The compound caused the mice led to increase the rate at which they burned calories...
Sunday, January 02, 2011
Have heart disease? Perhaps dad's diet is to blame
For the past few years, a slew of studies have focused attention on the role that a pregnant woman's diet has on the future health of her offspring. I previously warned women off doughnuts and Big Macs in this article citing research showing that pregnant women who dined on junk food could increase their baby's chances of developing diabetes and heart disease later in life.
That's because certain environmental factors -- like how much weight a woman gains when she's pregnant, what she eats and what chemicals she's exposed to -- actually affect how her baby's genes are programmed in the womb.
Well, now it's time for dads to share some of the blame for faulty programming that wires kids for obesity and a host of other health ills. A study published last week in the journal Cell suggests that what a father eats before his offspring are created can have some influence on fetal programming for disease risk.
At least father mice, since that's what the researchers studied...
That's because certain environmental factors -- like how much weight a woman gains when she's pregnant, what she eats and what chemicals she's exposed to -- actually affect how her baby's genes are programmed in the womb.
Well, now it's time for dads to share some of the blame for faulty programming that wires kids for obesity and a host of other health ills. A study published last week in the journal Cell suggests that what a father eats before his offspring are created can have some influence on fetal programming for disease risk.
At least father mice, since that's what the researchers studied...
Japanese firm partners with local researchers to fight obesity
"In labs, we've cured obesity and diabetes in mice hundreds of times," Smith said. "But not all the things that work in mice work in people."...
Officials at Orlando's Sanford-Burnham Research Institute and Florida Hospital on Monday announced a major partnership with Asia's largest pharmaceutical company — an alliance that will explore new ways to treat obesity.
Takeda Pharmaceuticals, a Japanese firm that has made major investments in diabetes and obesity research, inked a two-year deal with the nonprofit biomedical research facility at Lake Nona and its joint venture with Florida Hospital, the Translational Research Institute for Metabolism and Diabetes.
The two-year collaboration includes research funding from Takeda, but officials involved in the agreement would not disclose the terms of the deal. However, Sanford-Burnham officials said the new alliance is one of the largest and most ambitious research partnerships that Takeda has conducted with the not-for-profit sector.
"In terms of their discovery types of partnerships, this is one of the most significant that they have ever established outside of Japan," said Dr. Daniel Kelly, scientific director of Sanford-Burnham's Lake Nona campus.
"We view this collaboration as an opportunity to further Takeda's goal of identifying targets for new therapeutics to treat obesity and its negative health consequences, including metabolic syndrome, diabetes and heart disease," said Dr. Paul Chapman, head of Takeda's pharmaceutical research division.
The partnership is a significant step for Sanford-Burnham's Lake Nona campus, said Russell Allen, president of BioFlorida, the state's biomedical industry association.
"Takeda is a large, well-known company," he said. "It does help validate that Sanford-Burnham in Orlando is conducting strong science because Takeda is not going to partner with just anyone."
Although most obesity drugs on the market today target the brain — in hopes of controlling a person's appetite — those types of drugs often have serious side effects, including depression. Researchers at Sanford Burnham and the Translational Research Institute are taking another approach: Trying to make a person's muscles burn more fat.
"We're looking at ways to turn on fat-burning," said Dr. Steven Smith, scientific director at the Translational Research Institute. "The idea is that we can help people lose weight by turning on the fat-burning and fat-oxidation mechanisms."
The earliest stages of the research will include studying the muscles of those who are obese and learning what makes their muscles different from everyone else's. That information will be used by scientists at Sanford-Burnham and Takeda to do lab research.
Officials at the three organizations began discussing a potential partnership in early 2010. Being able to test ideas on people — instead of lab mice — made the collaboration attractive to the scientists involved.
"In labs, we've cured obesity and diabetes in mice hundreds of times," Smith said....
Officials at Orlando's Sanford-Burnham Research Institute and Florida Hospital on Monday announced a major partnership with Asia's largest pharmaceutical company — an alliance that will explore new ways to treat obesity.
Takeda Pharmaceuticals, a Japanese firm that has made major investments in diabetes and obesity research, inked a two-year deal with the nonprofit biomedical research facility at Lake Nona and its joint venture with Florida Hospital, the Translational Research Institute for Metabolism and Diabetes.
The two-year collaboration includes research funding from Takeda, but officials involved in the agreement would not disclose the terms of the deal. However, Sanford-Burnham officials said the new alliance is one of the largest and most ambitious research partnerships that Takeda has conducted with the not-for-profit sector.
"In terms of their discovery types of partnerships, this is one of the most significant that they have ever established outside of Japan," said Dr. Daniel Kelly, scientific director of Sanford-Burnham's Lake Nona campus.
"We view this collaboration as an opportunity to further Takeda's goal of identifying targets for new therapeutics to treat obesity and its negative health consequences, including metabolic syndrome, diabetes and heart disease," said Dr. Paul Chapman, head of Takeda's pharmaceutical research division.
The partnership is a significant step for Sanford-Burnham's Lake Nona campus, said Russell Allen, president of BioFlorida, the state's biomedical industry association.
"Takeda is a large, well-known company," he said. "It does help validate that Sanford-Burnham in Orlando is conducting strong science because Takeda is not going to partner with just anyone."
Although most obesity drugs on the market today target the brain — in hopes of controlling a person's appetite — those types of drugs often have serious side effects, including depression. Researchers at Sanford Burnham and the Translational Research Institute are taking another approach: Trying to make a person's muscles burn more fat.
"We're looking at ways to turn on fat-burning," said Dr. Steven Smith, scientific director at the Translational Research Institute. "The idea is that we can help people lose weight by turning on the fat-burning and fat-oxidation mechanisms."
The earliest stages of the research will include studying the muscles of those who are obese and learning what makes their muscles different from everyone else's. That information will be used by scientists at Sanford-Burnham and Takeda to do lab research.
Officials at the three organizations began discussing a potential partnership in early 2010. Being able to test ideas on people — instead of lab mice — made the collaboration attractive to the scientists involved.
"In labs, we've cured obesity and diabetes in mice hundreds of times," Smith said....
Obesity caused by what you breathe?
Diabetes. Asthma. Obesity. All are on the rise. What if they're all caused by the same thing?
At least one study found that air pollution — known to contribute to asthma — also spurs both obesity and diabetes in young mice, suggesting that it may also contribute to the ubiquitous problems in humans.
Ohio State researchers found that young mice exposed to air pollution had larger and more fat cells in their abdominal area and higher blood sugar levels than mice eating the same diet but breathing clean air...
At least one study found that air pollution — known to contribute to asthma — also spurs both obesity and diabetes in young mice, suggesting that it may also contribute to the ubiquitous problems in humans.
Ohio State researchers found that young mice exposed to air pollution had larger and more fat cells in their abdominal area and higher blood sugar levels than mice eating the same diet but breathing clean air...
Subscribe to:
Posts (Atom)