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...
Tuesday, August 30, 2011
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...
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