For years, it has been assumed that obesity led to type 2 diabetes by causing inflammation, which was thought to change the way the body reacts to the effects of insulin. However, a new study suggests that this hypothesis may need an update.
Researchers from Children’s Hospital Boston reported in the journal Nature Medicine that inflammation actually activates two different proteins that play key roles in stablizing blood sugar levels. Without the presence of inflammation, these proteins remain dormant.
The findings suggest an important new role for inflammation in the body. Rather than being the cause of health problems like type 2 diabetes, heart disease and certain cancers, it may actually be a helpful reaction to other conditions in the body that are the real cause of disease...
Sunday, October 09, 2011
Cold mice might be skewing weight-loss drug studies
Animals and people burn calories in an effort to keep warm, and room temperature may be affecting the testing and development of weight-loss drugs, says University of Alabama at Birmingham researcher Daniel Smith, Ph.D.
Smith, an instructor in the Department of Nutrition Sciences, received a 2011 Early-Career Research Grant from The Obesity Society for his proposal to examine the effect of room temperature on obesity-related drug effects in mice.
“More than 90 percent of weight-loss drugs that show promising results in lab tests fail to reach approval for treatment in humans,” said Smith. “There appears to be a translation gap from the bench to the market. I think the temperature used in animal research facilities may be part of the reason.”
Smith noted that most animals are tested in rooms where the temperature is near 22 degrees Celsius (72F), which is comfortable for most adult humans. However, that temperature is cold for mice, which have to eat more to elevate their metabolic rate to meet the constant, cold stress.
“If you raise the temperature to 30 degrees Celsius, that puts the mice in their thermo-neutral zone or a comfortable temperature for them, mimicking more closely what humans experience in modern daily life,” said Smith.
Smith will test a handful of weight-loss drugs in a group of mice housed at 22 degrees Celsius and another group at 30 degrees Celsius. Food intake, body weight and body composition will be measured to determine drug-related, weight-loss effects in the two temperatures. He said this study could be an important turning point for obesity researchers using animal models.
“This could change the models of pre-clinical drug testing,” said Smith...
Smith, an instructor in the Department of Nutrition Sciences, received a 2011 Early-Career Research Grant from The Obesity Society for his proposal to examine the effect of room temperature on obesity-related drug effects in mice.
“More than 90 percent of weight-loss drugs that show promising results in lab tests fail to reach approval for treatment in humans,” said Smith. “There appears to be a translation gap from the bench to the market. I think the temperature used in animal research facilities may be part of the reason.”
Smith noted that most animals are tested in rooms where the temperature is near 22 degrees Celsius (72F), which is comfortable for most adult humans. However, that temperature is cold for mice, which have to eat more to elevate their metabolic rate to meet the constant, cold stress.
“If you raise the temperature to 30 degrees Celsius, that puts the mice in their thermo-neutral zone or a comfortable temperature for them, mimicking more closely what humans experience in modern daily life,” said Smith.
Smith will test a handful of weight-loss drugs in a group of mice housed at 22 degrees Celsius and another group at 30 degrees Celsius. Food intake, body weight and body composition will be measured to determine drug-related, weight-loss effects in the two temperatures. He said this study could be an important turning point for obesity researchers using animal models.
“This could change the models of pre-clinical drug testing,” said Smith...
Parents' weight affects children, study shows
Overweight parents are more likely to have children who are obese which could lead to the need for weight loss surgery, according to a new study.
Thinner children are therefore more likely to come from slimmer families, researchers at University College London (UCL) have found through a national health survey for England.
Published in the Archives of Pediatrics & Adolescent Medicine, the study found that there is a strong association between children's and parents' body size.
When both parents were in the thinner half of the healthy weight range, the chance of the child being thin was 16.2 per cent, compared with 7.8 per cent when both parents were in the upper half of range.
In comparison, 5.3 per cent of children with two overweight parents are likely to be thin.
Lead author Dr Katriina Whitaker, UCL epidemiology and public health specialist, commented: "We know from other studies that children's weights are correlated with those of their parents, but previous research has tended to focus on obesity rather than the other end of the spectrum."
A further study published in Obesity suggested that green tea could decrease the risk of obesity after lab tests on mice showed positive results...
Thinner children are therefore more likely to come from slimmer families, researchers at University College London (UCL) have found through a national health survey for England.
Published in the Archives of Pediatrics & Adolescent Medicine, the study found that there is a strong association between children's and parents' body size.
When both parents were in the thinner half of the healthy weight range, the chance of the child being thin was 16.2 per cent, compared with 7.8 per cent when both parents were in the upper half of range.
In comparison, 5.3 per cent of children with two overweight parents are likely to be thin.
Lead author Dr Katriina Whitaker, UCL epidemiology and public health specialist, commented: "We know from other studies that children's weights are correlated with those of their parents, but previous research has tended to focus on obesity rather than the other end of the spectrum."
A further study published in Obesity suggested that green tea could decrease the risk of obesity after lab tests on mice showed positive results...
Carbs may suppress fat absorption and accumulation: Animal data
Dietary fructooligosaccharides – carbohydrates with established prebiotic activity – may suppress high-fat diet-induced body fat accumulation, and inhibit intestinal absorption of dietary fats, say researchers.
Writing in the journal BioFactors, researchers investigated the effects of fructooligosaccharides (FOS) on the development of obesity, using two experiments in rats and mice. They found that body weight and percent body fat were lower in mice fed FOS than in controls, whilst rats receiving an oral dose of FOS were reported to have suppressed elevation of plasma triglycerides.
“We have shown that a low dose of dietary FOS suppressed weight gain, accumulation of visceral adipose [fat] tissue, and the increase in liver triglycerides resulting from feeding a high-fat ‘western’ diet ... while fat excretion increased,” reported the authors, led by Yuko Nakamura from the Food and Health R&D Laboratories at the Japanese pharmaceutical company Meiji Seika Kaisha.
“These results suggest that FOS may prevent fat accumulation by inhibiting intestinal absorption of dietary fat in a high-fat ‘western’ diet,” added the researchers...
Writing in the journal BioFactors, researchers investigated the effects of fructooligosaccharides (FOS) on the development of obesity, using two experiments in rats and mice. They found that body weight and percent body fat were lower in mice fed FOS than in controls, whilst rats receiving an oral dose of FOS were reported to have suppressed elevation of plasma triglycerides.
“We have shown that a low dose of dietary FOS suppressed weight gain, accumulation of visceral adipose [fat] tissue, and the increase in liver triglycerides resulting from feeding a high-fat ‘western’ diet ... while fat excretion increased,” reported the authors, led by Yuko Nakamura from the Food and Health R&D Laboratories at the Japanese pharmaceutical company Meiji Seika Kaisha.
“These results suggest that FOS may prevent fat accumulation by inhibiting intestinal absorption of dietary fat in a high-fat ‘western’ diet,” added the researchers...
Discover Key Protein Responsible for Fat Storage
UC Davis Health System researchers have discovered that a protein called galectin-12 plays a key role in fat storage, a finding that could lead to improvements in treating obesity and diabetes. The researchers found that without the ability to make the protein, mice used in their research investigation stored 40 percent less body fat and had increased fat metabolism and decreased insulin resistance.
"This study for the first time demonstrates the importance of a galectin in energy metabolism," said Fu-Tong Liu, distinguished professor and chair of the UC Davis Department of Dermatology, and senior author on the paper.
The findings, published online this week in the early edition of the Proceedings of the National Academy of Sciences, point to galectin-12 as a potential target for the treatment of obesity and diabetes in humans. The breakdown and storage of fat in the body are both tightly controlled processes that involve numerous chemical signals, Liu said.
"In this case, galectin-12 seems to be signaling to fat cells that its time to conserve rather than burn energy," he said. "If we can interrupt that signal, we have a chance at improving fat metabolism and reducing insulin resistance in patients with obesity and type 2 diabetes."
Obesity is the number-one predictor for the development of diabetes, a leading cause of death and disability in the United States. An estimated 24 million Americans have the disease. Between 90 and 95 percent of them have type 2 diabetes, and about 80 percent of people with type 2 diabetes are overweight or obese.
In its early stages, type 2 diabetes is characterized by insulin resistance. The pancreas is producing insulin, but for unknown reasons the body cannot use the insulin effectively. After several years, insulin production decreases, glucose builds up in the blood and the body cannot make efficient use of its main source of fuel. People with advanced diabetes may experience blindness, require limb amputations or suffer fatal organ failure.
In order to discover potential treatments for type 2 diabetes, Liu and his UC Davis colleagues have been working to understand the chemical signals involved in normal energy metabolism and storage. They isolated and cloned the galectin-12 gene 10 years ago. Since then, their studies have shown that the gene is preferentially expressed in fat cells, and that its expression is required for fat-cell differentiation. To enable a focus on specific biological mechanisms associated with galectin-12, the researchers worked with the UC Davis Mouse Biology Program to obtain genetically customized mice that have had individual genes systematically turned off or "knocked out."
"We decided to create the galectin-12 knockout mice to further clarify the function of this protein in animals," said Ri-Yao Yang, associate project scientist...
"This study for the first time demonstrates the importance of a galectin in energy metabolism," said Fu-Tong Liu, distinguished professor and chair of the UC Davis Department of Dermatology, and senior author on the paper.
The findings, published online this week in the early edition of the Proceedings of the National Academy of Sciences, point to galectin-12 as a potential target for the treatment of obesity and diabetes in humans. The breakdown and storage of fat in the body are both tightly controlled processes that involve numerous chemical signals, Liu said.
"In this case, galectin-12 seems to be signaling to fat cells that its time to conserve rather than burn energy," he said. "If we can interrupt that signal, we have a chance at improving fat metabolism and reducing insulin resistance in patients with obesity and type 2 diabetes."
Obesity is the number-one predictor for the development of diabetes, a leading cause of death and disability in the United States. An estimated 24 million Americans have the disease. Between 90 and 95 percent of them have type 2 diabetes, and about 80 percent of people with type 2 diabetes are overweight or obese.
In its early stages, type 2 diabetes is characterized by insulin resistance. The pancreas is producing insulin, but for unknown reasons the body cannot use the insulin effectively. After several years, insulin production decreases, glucose builds up in the blood and the body cannot make efficient use of its main source of fuel. People with advanced diabetes may experience blindness, require limb amputations or suffer fatal organ failure.
In order to discover potential treatments for type 2 diabetes, Liu and his UC Davis colleagues have been working to understand the chemical signals involved in normal energy metabolism and storage. They isolated and cloned the galectin-12 gene 10 years ago. Since then, their studies have shown that the gene is preferentially expressed in fat cells, and that its expression is required for fat-cell differentiation. To enable a focus on specific biological mechanisms associated with galectin-12, the researchers worked with the UC Davis Mouse Biology Program to obtain genetically customized mice that have had individual genes systematically turned off or "knocked out."
"We decided to create the galectin-12 knockout mice to further clarify the function of this protein in animals," said Ri-Yao Yang, associate project scientist...
Gene clue to diabetes sufferers
Scientists have identified a gene that could explain why some people are more susceptible than others to diabetes.
The gene, found in tests on obese mice, controls a protein called tomosyn-2 which acts as a brake on insulin secretion from the pancreas, the researchers also discovered.
Insulin is made and released by beta cells in the pancreas and regulates blood sugars. Those with type 1 diabetes have too little insulin, while those with type 2 are insulin-resistant - both conditions potentially causing serious health problems if they are not treated.
Alan Attie, of the University of Wisconsin-Madison, who led the study, said: "It's too early for us to know how relevant this gene will be to human diabetes, but the concept of negative regulation is one of the most interesting things to come out of this study and that very likely applies to humans."
The researchers studied obese mice as it takes more insulin to lower glucose for an obese person than someone of a healthy weight...
The gene, found in tests on obese mice, controls a protein called tomosyn-2 which acts as a brake on insulin secretion from the pancreas, the researchers also discovered.
Insulin is made and released by beta cells in the pancreas and regulates blood sugars. Those with type 1 diabetes have too little insulin, while those with type 2 are insulin-resistant - both conditions potentially causing serious health problems if they are not treated.
Alan Attie, of the University of Wisconsin-Madison, who led the study, said: "It's too early for us to know how relevant this gene will be to human diabetes, but the concept of negative regulation is one of the most interesting things to come out of this study and that very likely applies to humans."
The researchers studied obese mice as it takes more insulin to lower glucose for an obese person than someone of a healthy weight...
Green Tea May Help You Lose Weight
Drinking green tea can slow down weight gain by limiting the amount of fat absorbed by the body, the Daily Mail reported Wednesday.
In a new study, Penn State University researchers found that a compound in the herbal tea slowed down weight gain in mice.
Crucially, the mice were already obese at the start of the experiment. This makes the findings more relevant to humans because people often consider dietary changes only when they notice problems associated with obesity, the researchers said...
In a new study, Penn State University researchers found that a compound in the herbal tea slowed down weight gain in mice.
Crucially, the mice were already obese at the start of the experiment. This makes the findings more relevant to humans because people often consider dietary changes only when they notice problems associated with obesity, the researchers said...
Scientists identify genes involved in storing fat
Researchers funded by the Wellcome Trust have identified several genes in fat tissue that may lead us to retain fat unnecessarily in the body. The study, using a mouse model, may explain why some people carry more weight than others even when they have similar diets because of genes that encourage fat storage.
Scientists at the University of Edinburgh compared fat tissue from mice that had been selectively bred for many generations to be increasingly fat or thin, and as a result had acquired weight-related genes. The research, published in the journal ’PLoS One’, cross-referenced thousands of genes and pinpointed genes that prevented the breakdown of fat, which were more prevalent in the fat tissue of the overweight mice than in the fat tissue of the lean mice.
Mice were then bred from one overweight parent and one lean parent. Those among the offspring that were born overweight were found to have the same active genes as the fatter parent mice - an indication that hereditary factors play a part in fat storage and can increase the likelihood of putting on weight.
The research also found that the thin offspring had an added protection against weight gain. When both sets of mice were given fatty foods, the thin offspring seemed able to break down fatty tissue more easily than the heavier mice, suggesting they had inherited ’lean genes’...
Scientists at the University of Edinburgh compared fat tissue from mice that had been selectively bred for many generations to be increasingly fat or thin, and as a result had acquired weight-related genes. The research, published in the journal ’PLoS One’, cross-referenced thousands of genes and pinpointed genes that prevented the breakdown of fat, which were more prevalent in the fat tissue of the overweight mice than in the fat tissue of the lean mice.
Mice were then bred from one overweight parent and one lean parent. Those among the offspring that were born overweight were found to have the same active genes as the fatter parent mice - an indication that hereditary factors play a part in fat storage and can increase the likelihood of putting on weight.
The research also found that the thin offspring had an added protection against weight gain. When both sets of mice were given fatty foods, the thin offspring seemed able to break down fatty tissue more easily than the heavier mice, suggesting they had inherited ’lean genes’...
Fat content in mice affected by environment
A recent study found that mice living in socially enriching environments converted a greater portion of their energy-storing white fat to energy-burning brown fat, losing weight despite their increased caloric intake. These findings reinforce how social and physical environments can impact animal metabolisms.
Adipose tissue, commonly known as fat, comes in two types: white and brown. White fat, which constitutes as much as 20 percent of the body weight in men and 25 percent of the body weight in women, serves to store excess energy, cushion organs and maintain body temperature. Brown fat, which is especially abundant in newborns and hibernating mammals, expends energy to generate heat. Increases in white fat and brown fat concentrations are associated with weight gain and loss, respectively.
Functional differences between white and brown fat are predicted by differences in structure. White adipocytes contain a single, large lipid droplet that occupies most of the cell volume. In contrast, brown adipocytes contain numerous small droplets, more iron-containing mitochondria, which explains the characteristic brown color, and more capillaries to deliver greater amounts of oxygen.
While brown fat is best known for its role in insulating infants, scientists found that active brown fat is also present in adults. In addition, cold exposure and activation of the sympathetic nervous system drives the production of more brown fat. The new study, whose results are published in the September issue of Cell Metabolism, suggests that an engaging environment can provide another, perhaps more effective means to increase brown fat.
According to Lei Cao of The Ohio State University, the typical laboratory mouse leads what might be considered a "couch potato" lifestyle. Lab mice are given free access to food and water, as well as a few potential playmates. However, they are not given much else to do.
In the enriched environment, mice live in groups of 15 to 20. They are given more space as well as exercise wheels, mazes and toys. After four weeks in the enriched environment, the mice's abdominal fat decreased by 50 percent...
Adipose tissue, commonly known as fat, comes in two types: white and brown. White fat, which constitutes as much as 20 percent of the body weight in men and 25 percent of the body weight in women, serves to store excess energy, cushion organs and maintain body temperature. Brown fat, which is especially abundant in newborns and hibernating mammals, expends energy to generate heat. Increases in white fat and brown fat concentrations are associated with weight gain and loss, respectively.
Functional differences between white and brown fat are predicted by differences in structure. White adipocytes contain a single, large lipid droplet that occupies most of the cell volume. In contrast, brown adipocytes contain numerous small droplets, more iron-containing mitochondria, which explains the characteristic brown color, and more capillaries to deliver greater amounts of oxygen.
While brown fat is best known for its role in insulating infants, scientists found that active brown fat is also present in adults. In addition, cold exposure and activation of the sympathetic nervous system drives the production of more brown fat. The new study, whose results are published in the September issue of Cell Metabolism, suggests that an engaging environment can provide another, perhaps more effective means to increase brown fat.
According to Lei Cao of The Ohio State University, the typical laboratory mouse leads what might be considered a "couch potato" lifestyle. Lab mice are given free access to food and water, as well as a few potential playmates. However, they are not given much else to do.
In the enriched environment, mice live in groups of 15 to 20. They are given more space as well as exercise wheels, mazes and toys. After four weeks in the enriched environment, the mice's abdominal fat decreased by 50 percent...
Tuesday, August 30, 2011
Black tea extract prevents obesity
There are many diets you can try to avoid or prevent obesity. But chances are good that none of them work for you. The problem is that most people couldn't control their daily intake of calories because foods with high fat, high salt and high sugar taste just too good.
New research suggests that simply taking some extract of a Chinese black tea called Pu-Erh tea after meals may help you stop gaining weight even if you continue eating a typical obesity-inducing Western diet full of high fat, high protein and high energy.
The research conducted by Yasuyuki Oi of Nippon Supplement, Inc. based out of Osaka, Japan found mice given the black tea extract in some dose did not raise levels of blood triglycerides after ingestion of a corn oil emulsion.
The researchers published the results in Phytotherapy Research. In the research, female ddy mice were given one of seven diets with either high fat, or a normal dietary composition, or supplemented black tea extract, or gallic acid in different doses for a period of 12 weeks...
New research suggests that simply taking some extract of a Chinese black tea called Pu-Erh tea after meals may help you stop gaining weight even if you continue eating a typical obesity-inducing Western diet full of high fat, high protein and high energy.
The research conducted by Yasuyuki Oi of Nippon Supplement, Inc. based out of Osaka, Japan found mice given the black tea extract in some dose did not raise levels of blood triglycerides after ingestion of a corn oil emulsion.
The researchers published the results in Phytotherapy Research. In the research, female ddy mice were given one of seven diets with either high fat, or a normal dietary composition, or supplemented black tea extract, or gallic acid in different doses for a period of 12 weeks...
Will new wonder drug let humans 'have their cake and eat it, too?'
Imagine a drug that combines an ingredient found in red wine, which extends your life on the provision you eat as much as you please, eventually becoming obese. Sound too good to be true? Those are the provisions of the new drug called SRT-1720, and the success found in obese lab mice has been amazing.
LOS ANGELES, CA (Catholic Online) - SRT-1720 is an experimental agent, which in different forms is also being tested in humans. The drug found to prevent some of the life-shortening diseases associated with obesity in mice, by curbing levels of fat in the liver and improving sensitivity to insulin.
SRT-1720 is based on the compound resveratrol, which is found in red wine and is thought to combat some of the effects of aging by boosting levels of proteins called sirtuins. These are the proteins that have been associated with 30 percent life extension in mice and rats put on low-calorie diets.
Developed by David Sinclair, a biologist at Harvard Medical School and one of the co-authors of the current mouse study, the findings associated with SRT-1720 appear in the new journal Scientific Reports...
LOS ANGELES, CA (Catholic Online) - SRT-1720 is an experimental agent, which in different forms is also being tested in humans. The drug found to prevent some of the life-shortening diseases associated with obesity in mice, by curbing levels of fat in the liver and improving sensitivity to insulin.
SRT-1720 is based on the compound resveratrol, which is found in red wine and is thought to combat some of the effects of aging by boosting levels of proteins called sirtuins. These are the proteins that have been associated with 30 percent life extension in mice and rats put on low-calorie diets.
Developed by David Sinclair, a biologist at Harvard Medical School and one of the co-authors of the current mouse study, the findings associated with SRT-1720 appear in the new journal Scientific Reports...
Slim down by targeting the hormone uroguanylin
The number of people who are obese and suffer one or more of its associated health problems (including type 2 diabetes) is escalating dramatically. Researchers are seeking to identify new targets for therapeutics that could limit appetite and thereby obesity. A team of researchers, led by Scott Waldman, at Thomas Jefferson University, Philadelphia, has now uncovered one such potential target by studying the molecular control of appetite in mice.
In the study, Waldman and colleagues found that nutrient intake by mice caused cells in their gut to secrete the precursor of the hormone uroguanylin (prouroguanylin) into the blood...
In the study, Waldman and colleagues found that nutrient intake by mice caused cells in their gut to secrete the precursor of the hormone uroguanylin (prouroguanylin) into the blood...
Genetics' new frontier: What mom eats, weighs in pregnancy can set child up for obesity, diabetes
Cracking the human genome is already old news for those riding the next wave of genetic research. The rising field of epigenetics is revealing how diet, behavior and the environment are reprogramming the genes we're dealt at conception.
Although your DNA was locked in the moment your parents' egg and sperm met, how those genes get expressed depends on what happened next. "Most chronic diseases that occur in adulthood have their origins in the first 1,000 days after conception," said Kent Thornburg, an epigenetics researcher at Oregon Health and Science University.
What's more, the epigenetic changes that happen in the womb get passed on to future generations.
Sorry, moms. That means once again, the pressure is on you.
"If your mom was obese while she was pregnant with you, you're marked," said Philip Wood, professor at Sanford Burnham Research Institute in Lake Nona. You will have an uphill battle fighting off excess weight and its ill effects, including diabetes and heart disease, even if you're adopted and raised by slim parents, he said.
The findings are significant as medical science works to identify causes and cures for the two most serious and costly epidemics facing America: obesity and diabetes.
We don't understand all of the mechanisms, but they likely involve maternal circulating hormones, such as leptin and insulin, and glucose levels that can alter how the placenta develops and what nutrients cross it, said Tracy Bale, associate professor of neuroscience at the University of Pennsylvania School of Veterinary Medicine, who has done epigenetic studies on animals.
Studies have shown that these effects can be handed down to the next generation, she added.
Rewriting the script
Epigenetics can silence or draw out the expression of genes.
"If DNA is the hardware, epigenetics is the software that tells genes what to do," said Randy Jirtle, an epigenetics researcher at Duke University Medical Center.
A study conducted on mice, and published in 2003 in Molecular Cell Biology, illustrated the effects of diet on genes. The mice in the study carried the agouti gene, which humans also have.
When scientists fed pregnant mice a certain diet that silenced the gene, the baby mice came out yellow, fat and prone to diabetes and cancer. When they fed the mice diets that activated the gene — a diet rich in folic acid, B vitamins and choline — mice came out skinny, brown and not susceptible to disease.
"The mice were genetically identical," said Jirtle, who was part of the study. "The only difference was what the mothers ate."
Granted these are mice, not humans, he added, "but the experiment showed that a mother's diet can shape the epigenome of her offspring."...
Although your DNA was locked in the moment your parents' egg and sperm met, how those genes get expressed depends on what happened next. "Most chronic diseases that occur in adulthood have their origins in the first 1,000 days after conception," said Kent Thornburg, an epigenetics researcher at Oregon Health and Science University.
What's more, the epigenetic changes that happen in the womb get passed on to future generations.
Sorry, moms. That means once again, the pressure is on you.
"If your mom was obese while she was pregnant with you, you're marked," said Philip Wood, professor at Sanford Burnham Research Institute in Lake Nona. You will have an uphill battle fighting off excess weight and its ill effects, including diabetes and heart disease, even if you're adopted and raised by slim parents, he said.
The findings are significant as medical science works to identify causes and cures for the two most serious and costly epidemics facing America: obesity and diabetes.
We don't understand all of the mechanisms, but they likely involve maternal circulating hormones, such as leptin and insulin, and glucose levels that can alter how the placenta develops and what nutrients cross it, said Tracy Bale, associate professor of neuroscience at the University of Pennsylvania School of Veterinary Medicine, who has done epigenetic studies on animals.
Studies have shown that these effects can be handed down to the next generation, she added.
Rewriting the script
Epigenetics can silence or draw out the expression of genes.
"If DNA is the hardware, epigenetics is the software that tells genes what to do," said Randy Jirtle, an epigenetics researcher at Duke University Medical Center.
A study conducted on mice, and published in 2003 in Molecular Cell Biology, illustrated the effects of diet on genes. The mice in the study carried the agouti gene, which humans also have.
When scientists fed pregnant mice a certain diet that silenced the gene, the baby mice came out yellow, fat and prone to diabetes and cancer. When they fed the mice diets that activated the gene — a diet rich in folic acid, B vitamins and choline — mice came out skinny, brown and not susceptible to disease.
"The mice were genetically identical," said Jirtle, who was part of the study. "The only difference was what the mothers ate."
Granted these are mice, not humans, he added, "but the experiment showed that a mother's diet can shape the epigenome of her offspring."...
Saturday, August 27, 2011
How fatty food triggers diabetes: Scientists believe discovery paves way for Type 2 'cure'
Fatty food trips a genetic switch in the body that can trigger diabetes, a study has found.
Understanding the biological pathway could lead to a potential cure for the disease, say scientists.
The discovery helps explain why Type 2 diabetes is so often linked to obesity.
In studies of mice and humans, researchers found that high levels of fat disrupted two key proteins that turn genes on and off...
Understanding the biological pathway could lead to a potential cure for the disease, say scientists.
The discovery helps explain why Type 2 diabetes is so often linked to obesity.
In studies of mice and humans, researchers found that high levels of fat disrupted two key proteins that turn genes on and off...
Fat Mice Live Longer With Novel Drug
An investigational compound extended survival in middle-age, obese male mice that were eating a high-fat diet, but researchers warned that it was too soon to say if the drug could do the same for humans.
Three groups of mice all gained a similar amount of weight during the study, but those that ate a low dose of SRT1720 lived 4% longer and those that ate a high dose lived 18% longer than their untreated counterparts (P<0.001), Rafael de Cabo, PhD, of the National Institute on Aging's Laboratory of Experimental Gerontology in Baltimore, and colleagues, wrote online in Scientific Reports...
Three groups of mice all gained a similar amount of weight during the study, but those that ate a low dose of SRT1720 lived 4% longer and those that ate a high dose lived 18% longer than their untreated counterparts (P<0.001), Rafael de Cabo, PhD, of the National Institute on Aging's Laboratory of Experimental Gerontology in Baltimore, and colleagues, wrote online in Scientific Reports...
Saturday, August 20, 2011
Compound improves health, increases lifespan of obese mice
Researchers have reported that obese male mice treated with a synthetic compound called SRT1720 were healthier and lived longer compared to non-treated obese mice. The experimental compound was found to improve the function of the liver, pancreas and heart in mice.
The National Institute on Aging (NIA) supported the study, in collaboration with Sirtris, a GlaxoSmithKline company. The study was primarily conducted by the NIA, part of the National Institutes of Health, and is published online in the Thursday, August 18, 2011, issue of Scientific Reports.
"This study has interesting implications for research on the biology of aging. It demonstrates that years of healthy life can be extended in an animal model of diet-induced obesity by a synthetic compound that modulates a gene pathway associated with aging," said NIA Director Richard J. Hodes, M.D. More research is needed to assess the relevance of these findings in people, Hodes and the researchers noted.
SRT1720, a patented molecule, has been shown to activate the SIRT1enzyme, part of a class of enzymes called sirtuins. Sirtuins have been previously implicated in aging processes and are thought to contribute to the positive effects of dietary restriction (also known as calorie restriction) in higher organisms, including nonhuman primates.
In this study, scientists compared the health of 1-year-old, or middle-aged, male mice fed a high-fat diet with a high dose of SRT1720, a low dose of SRT1720 or no SRT1720. Additionally, these mice were compared to a control group of 1-year-old male mice fed a standard diet...
The National Institute on Aging (NIA) supported the study, in collaboration with Sirtris, a GlaxoSmithKline company. The study was primarily conducted by the NIA, part of the National Institutes of Health, and is published online in the Thursday, August 18, 2011, issue of Scientific Reports.
"This study has interesting implications for research on the biology of aging. It demonstrates that years of healthy life can be extended in an animal model of diet-induced obesity by a synthetic compound that modulates a gene pathway associated with aging," said NIA Director Richard J. Hodes, M.D. More research is needed to assess the relevance of these findings in people, Hodes and the researchers noted.
SRT1720, a patented molecule, has been shown to activate the SIRT1enzyme, part of a class of enzymes called sirtuins. Sirtuins have been previously implicated in aging processes and are thought to contribute to the positive effects of dietary restriction (also known as calorie restriction) in higher organisms, including nonhuman primates.
In this study, scientists compared the health of 1-year-old, or middle-aged, male mice fed a high-fat diet with a high dose of SRT1720, a low dose of SRT1720 or no SRT1720. Additionally, these mice were compared to a control group of 1-year-old male mice fed a standard diet...
Sunday, August 14, 2011
Brown Fat, Also Known As Good Fat, More Common In Leaner Children
Investigators at Joslin Diabetes Center and Children's Hospital Boston have revealed that a type of "good" fat known as brown fat occurs in varying amounts in children which increases until puberty and then declines. Brown fat is more common in children who are leaner...
In 2010 a Joslin investigation identified cells in mice that can be triggered to transform into brown fat....
In 2010 a Joslin investigation identified cells in mice that can be triggered to transform into brown fat....
Brain Protein ‘Nesfatin-1’ Shows Promise In Checking Obesity
Study conducted by an Indian-origin researcher showed that protein present in human brain may actually hold the key to keeping hunger and blood glucose in hand and keep unwanted pounds away.
Associate professor in biology at Canada's York University, Suraj Unniappan is investigating the metabolic effects of a protein known as nesfatin-1 present within the human brain.
Prof Suraj discovered that rats fed nesfatin-1 consumed less, utilized extra stored fat and turned more active.
In addition, it induced insulin discharge from the pancreatic beta cells of both rats and mice...
Associate professor in biology at Canada's York University, Suraj Unniappan is investigating the metabolic effects of a protein known as nesfatin-1 present within the human brain.
Prof Suraj discovered that rats fed nesfatin-1 consumed less, utilized extra stored fat and turned more active.
In addition, it induced insulin discharge from the pancreatic beta cells of both rats and mice...
York U Researchers Zero In On Protein That May Help Treat Obesity, Diabetes
A newly-identified protein may hold the key to keeping appetite and blood sugar in check, according to a study by York University researchers.
Suraj Unniappan, associate professor in York's Department of Biology, Faculty of Science & Engineering, is delving into the metabolic effects of a protein called nesfatin-1, abundantly present in the brain. His studies found that rats administered with nesfatin-1 ate less, used more stored fat and became more active. In addition, the protein stimulated insulin secretion from the pancreatic beta cells of both rats and mice.
"[The rats] actually ate more frequently but in lesser amounts," says Unniappan, a member of York's neuroscience graduate diploma program, and a recipient of a Canadian Institutes of Health Research (CIHR) New Investigator Award. "In addition, they were more active and we found that their fatty acid oxidization was increased. In other words, the energy reserve being preferably used during nesfatin-1 treatment was fat. This suggests more fat loss, which could eventually result in body weight loss," he says....
Suraj Unniappan, associate professor in York's Department of Biology, Faculty of Science & Engineering, is delving into the metabolic effects of a protein called nesfatin-1, abundantly present in the brain. His studies found that rats administered with nesfatin-1 ate less, used more stored fat and became more active. In addition, the protein stimulated insulin secretion from the pancreatic beta cells of both rats and mice.
"[The rats] actually ate more frequently but in lesser amounts," says Unniappan, a member of York's neuroscience graduate diploma program, and a recipient of a Canadian Institutes of Health Research (CIHR) New Investigator Award. "In addition, they were more active and we found that their fatty acid oxidization was increased. In other words, the energy reserve being preferably used during nesfatin-1 treatment was fat. This suggests more fat loss, which could eventually result in body weight loss," he says....
Medical: In the obesity battle, it's mind over stomach
...Last winter, Baylor College of Medicine scientists reported working with mice genetically modified to lack a receptor for the ghrelin hormone.
They found this turned up the fat-burning thermostat in the animals' bodies. In an older group of the mice, the rodents were slimmer than a control group even though they ate just as much and were no more physically active.
Still another mouse study, reported in this month's Cell Metabolism, looked more closely at what happens inside the hypothalamus and found that when they are starved, some neurons in that part of the brain actually start eating bits of themselves, which in turn ramps up hormonal signals to start eating.
Such cellular cannibalism goes on all the time as part of the body's natural housekeeping, but the discovery that this process also helps regulate appetite opens a new possible route for obesity-fighting drugs....
They found this turned up the fat-burning thermostat in the animals' bodies. In an older group of the mice, the rodents were slimmer than a control group even though they ate just as much and were no more physically active.
Still another mouse study, reported in this month's Cell Metabolism, looked more closely at what happens inside the hypothalamus and found that when they are starved, some neurons in that part of the brain actually start eating bits of themselves, which in turn ramps up hormonal signals to start eating.
Such cellular cannibalism goes on all the time as part of the body's natural housekeeping, but the discovery that this process also helps regulate appetite opens a new possible route for obesity-fighting drugs....
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