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...
Wednesday, June 22, 2011
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...
Sunday, December 26, 2010
VITAMIN D REDUCES OBESITY-INDUCED UTERINE CANCER
FINDINGS FROM AN ANIMAL study by Georgetown researchers suggest obese women can reduce their risk of endometrial cancer by taking vitamin D supplements.
Scientists from Georgetown’s Lombardi Comprehensive Cancer Center recently showed that 67 percent of obese mice fed a regular diet developed this cancer, versus only 25 percent of obese mice fed a vitamin D-supplemented diet...
Scientists from Georgetown’s Lombardi Comprehensive Cancer Center recently showed that 67 percent of obese mice fed a regular diet developed this cancer, versus only 25 percent of obese mice fed a vitamin D-supplemented diet...
Could tea help with obesity treatment?
People undergoing obesity treatment could benefit from drinking tea.
A recent research project has revealed that tea can help to restrict weight gain and limit the negative health impact of fatty foods.
Conducted at Kobe University in Japan, the study looked at a group of mice fed either a normal diet or a high-fat diet.
The mice were also given water, black tea or green tea over a 14-week period.
Results showed that the mice that were drinking tea had suppressed body weight gain in comparison to the group on water.
In addition, black tea was found to counteract the harmful effects of the fat on the blood.
Dr Carrie Ruxton from the industry-backed Tea Advisory Panel explained: "This study is good news for tea drinkers, particularly those who drink black tea.
"Though the findings need to be confirmed in human studies...
A recent research project has revealed that tea can help to restrict weight gain and limit the negative health impact of fatty foods.
Conducted at Kobe University in Japan, the study looked at a group of mice fed either a normal diet or a high-fat diet.
The mice were also given water, black tea or green tea over a 14-week period.
Results showed that the mice that were drinking tea had suppressed body weight gain in comparison to the group on water.
In addition, black tea was found to counteract the harmful effects of the fat on the blood.
Dr Carrie Ruxton from the industry-backed Tea Advisory Panel explained: "This study is good news for tea drinkers, particularly those who drink black tea.
"Though the findings need to be confirmed in human studies...
Researchers Turn White Fat to Energy-Burning Brown Fat in Mice
Certain cells in white fat can be changed into energy-burning brown fat, according to an animal study that might one day lead to new treatments for obesity, researchers report.
In tests on mice, a team at the Joslin Diabetes Center in Boston found that exposure to a protein called BMP-7 caused progenitor cells in subcutaneous (just beneath the skin) white fat tissue and skeletal muscle to turn into brown fat cells...
In tests on mice, a team at the Joslin Diabetes Center in Boston found that exposure to a protein called BMP-7 caused progenitor cells in subcutaneous (just beneath the skin) white fat tissue and skeletal muscle to turn into brown fat cells...
Tuesday, December 21, 2010
Novel Weight-Loss Therapies? Scientists Identify Cells in Mice That Can Transform Into Energy-Burning Brown Fat
In some adults, the white fat cells that we all stockpile so readily are supplemented by a very different form of fat -- brown fat cells, which can offer the neat trick of burning energy rather than storing it. Researchers at Joslin Diabetes Center, which last year led the way in demonstrating an active role for brown fat in adults, now have identified progenitor cells in mouse white fat tissue and skeletal muscle that can be transformed into brown fat cells...
Monday, December 20, 2010
Top 100 Stories of 2010 #8: Obesity Reaches Epidemic Proportions
On the research front, meanwhile, investigators are making some progress in grasping obesity’s causes. A provocative study published in Science in April 2010 suggests that a change in the bacterial population of the gut contributes to the risk of metabolic syndrome, which is characterized by elevated weight, blood pressure, blood sugar, and blood fat. Researchers led by Emory University pathologist Andrew Gewirtz found that mice genetically deficient in an immune system receptor have altered gut bacteria, eat more than normal mice do, and develop features of metabolic syndrome. However, Gewirtz says it is “unlikely that there will be a single causative bacterium for obesity as there
is for ulcers.”
New research suggests viruses could be the cause of the obesity epidemic
THE obesity epidemic seen in humans and their pets may be caused by more than rubbish diets and lack of exercise.
Some scientists think it may be due to a combination of issues, including viruses or something else that affects cells or organs.
This is opposed to the commonly held belief based on poor Western lifestyles that feature over-eating, little exercise and fatty foods.
Scientists' curiosity was triggered when they noticed laboratory rats and mice on strict diets had put on weight just as domestic pets and feral animals living around humans had...
Some scientists think it may be due to a combination of issues, including viruses or something else that affects cells or organs.
This is opposed to the commonly held belief based on poor Western lifestyles that feature over-eating, little exercise and fatty foods.
Scientists' curiosity was triggered when they noticed laboratory rats and mice on strict diets had put on weight just as domestic pets and feral animals living around humans had...
Too fat? Study fingers one "thrifty gene" suspect
Looking beyond obvious causes of obesity like overeating, scientists said on Wednesday they may have found a gene that also plays a role, one that helped our ancestors survive famines.
Targeting this thrifty gene and others with diagnostic tests and drugs offers another way to fight the global epidemic of obesity, the researchers said.
Mice bred to lack this gene, known as CRTC3, can eat a high-fat diet without gaining weight, while normal mice on the same diet grow plump, the researchers found...
Targeting this thrifty gene and others with diagnostic tests and drugs offers another way to fight the global epidemic of obesity, the researchers said.
Mice bred to lack this gene, known as CRTC3, can eat a high-fat diet without gaining weight, while normal mice on the same diet grow plump, the researchers found...
Scientists Raise Fat-Burning Levels in Mice
Deleting the receptor of a protein known to promote obesity allowed mice to burn more fat, researchers report.
The role of the ghrelin protein in appetite and energy balance was discovered in 1999. This new finding suggests that ghrelin may not be as critical to energy expenditure as its cellular receptor, called growth hormone secretagogue receptor (GHS-R), explained Dr. Yuxiang Sun, of the Baylor College of Medicine in Houston.
That means that GHS-R might make a better target for treating obesity in humans.
In this study, Sun and colleagues found that deleting GHS-R from the body cells of mice prevented obesity by diminishing so-called "white fat" tissue and activating "brown fat" tissue, thereby increasing the production of fat-burning body heat...
The role of the ghrelin protein in appetite and energy balance was discovered in 1999. This new finding suggests that ghrelin may not be as critical to energy expenditure as its cellular receptor, called growth hormone secretagogue receptor (GHS-R), explained Dr. Yuxiang Sun, of the Baylor College of Medicine in Houston.
That means that GHS-R might make a better target for treating obesity in humans.
In this study, Sun and colleagues found that deleting GHS-R from the body cells of mice prevented obesity by diminishing so-called "white fat" tissue and activating "brown fat" tissue, thereby increasing the production of fat-burning body heat...
Tuesday, December 14, 2010
Deleting Ghrelin Receptor, but Not Ghrelin, Turns Up Fat-Burning Thermostat
Deleting the receptor, not the protein ghrelin itself, turns up the body's fat-burning thermostat, giving aging mice an exothermic boost toward a svelte physique, researchers reported at the American Society of Cell Biology's 50th Annual Meeting in Philadelphia.
The protein's receptor, growth hormone secretagogue receptor (GHS-R), might make a better target than ghrelin for treating obesity, according to Yuxiang Sun, M.D., Ph.D., of the Baylor College of Medicine in Houston, TX.
Sun said that experimentally deleting the receptor from the body cells of laboratory mice prevented obesity by diminishing white adipose tissues and activating brown adipose tissue, thereby increasing heat production.
The new finding that ghrelin may not be as critical to energy expenditure as its receptor, GHS-R, came from research on body temperature regulation at Baylor, Sun explained. GHS-R acts as the "lock" for the "key-like" ligand ghrelin to dock; GHS-R subsequently activates down-stream metabolic signal pathways...
The protein's receptor, growth hormone secretagogue receptor (GHS-R), might make a better target than ghrelin for treating obesity, according to Yuxiang Sun, M.D., Ph.D., of the Baylor College of Medicine in Houston, TX.
Sun said that experimentally deleting the receptor from the body cells of laboratory mice prevented obesity by diminishing white adipose tissues and activating brown adipose tissue, thereby increasing heat production.
The new finding that ghrelin may not be as critical to energy expenditure as its receptor, GHS-R, came from research on body temperature regulation at Baylor, Sun explained. GHS-R acts as the "lock" for the "key-like" ligand ghrelin to dock; GHS-R subsequently activates down-stream metabolic signal pathways...
Monday, December 13, 2010
Air pollution may increase risk of type 2 diabetes
Exposure to air pollution may increase the risk of developing obesity-related insulin resistance, which often progresses into type 2 diabetes, according to new research from Ohio State University.
Air pollution has been connected to a broad range of health problems, including cardiovascular dysfunction and certain types of cancer. However, the findings of the new research, which were published in the journal Arteriosclerosis, Thrombosis, and Vascular Biology are the first to indicate a potential link to diabetes.
For the study, researchers exposed adolescent mice to the sort of fine particulate air pollution that is commonly associated with automobile exhaust. When these animals reached adulthood, researchers found that they had higher levels of abdominal fat than normal mice.
"This is one of the first, if not the first, study to show that these fine particulates directly cause inflammation and changes in fat cells, both of which increase the risk for Type 2 diabetes," said Qinghua Sun, who led the investigation...
Air pollution has been connected to a broad range of health problems, including cardiovascular dysfunction and certain types of cancer. However, the findings of the new research, which were published in the journal Arteriosclerosis, Thrombosis, and Vascular Biology are the first to indicate a potential link to diabetes.
For the study, researchers exposed adolescent mice to the sort of fine particulate air pollution that is commonly associated with automobile exhaust. When these animals reached adulthood, researchers found that they had higher levels of abdominal fat than normal mice.
"This is one of the first, if not the first, study to show that these fine particulates directly cause inflammation and changes in fat cells, both of which increase the risk for Type 2 diabetes," said Qinghua Sun, who led the investigation...
Monday, December 06, 2010
Artificial light at night may cause obesity
...The present study compares three groups of lab mice. One was exposed to a "regular day" of 16 light hours and eight hours of dark. A second group was in continuous light for 24 hours and the third group was given regular light for 16 hours followed by eight hours of dimmed light. The three groups were placed in these conditions over the course of eight weeks and were given equal quantities of food.
The results show that the mice experiencing dimmed light and those exposed to 24 hours of light gained about 12 grams of body mass, while the mice exposed to the "regular day" only put on about eight grams of extra body mass - close to 50 percent less than the others.
The researchers observed that there was no difference in the amounts of food that all the mice ate, or in the extent of physical activity (monitored as locomotor activity). The lab tests also showed drastically reduced glucose tolerance in those mice exposed to LAN.
Another finding, which led to the second stage of the study, showed a significant difference between the groups in their timing of eating: The mice exposed to dimmed light ate 55% of their food during the "night" hours while those experiencing "regular days" ate only 36.5% of their food at night. This prompted the researchers to see whether this was the cause of the marked differences in body mass gain.
To do so, they gave the group of mice enjoying "regular days" and those exposed to dimmed light hours, three different options: Unlimited eating times; food only during the light hours; and food only during the "night" hours. There was no need to include the third group in this step of the research, as they did not have any "night" hours.
Nighttime TV can cause obesity
Once eating was limited to daytime only (which is when mice normally eat their food) or nighttime only (when they do not normally eat), there was no difference in body mass weight gain between the groups.
Haim explains that the study strengthens earlier findings by other researchers showing that exposure to LAN interferes with the production of melatonin - a hormone produced in the pineal gland in the brain under dark conditions at night. This interference causes changes in the body's cyclical functions and is what caused the mice to eat at abnormal hours...
The results show that the mice experiencing dimmed light and those exposed to 24 hours of light gained about 12 grams of body mass, while the mice exposed to the "regular day" only put on about eight grams of extra body mass - close to 50 percent less than the others.
The researchers observed that there was no difference in the amounts of food that all the mice ate, or in the extent of physical activity (monitored as locomotor activity). The lab tests also showed drastically reduced glucose tolerance in those mice exposed to LAN.
Another finding, which led to the second stage of the study, showed a significant difference between the groups in their timing of eating: The mice exposed to dimmed light ate 55% of their food during the "night" hours while those experiencing "regular days" ate only 36.5% of their food at night. This prompted the researchers to see whether this was the cause of the marked differences in body mass gain.
To do so, they gave the group of mice enjoying "regular days" and those exposed to dimmed light hours, three different options: Unlimited eating times; food only during the light hours; and food only during the "night" hours. There was no need to include the third group in this step of the research, as they did not have any "night" hours.
Nighttime TV can cause obesity
Once eating was limited to daytime only (which is when mice normally eat their food) or nighttime only (when they do not normally eat), there was no difference in body mass weight gain between the groups.
Haim explains that the study strengthens earlier findings by other researchers showing that exposure to LAN interferes with the production of melatonin - a hormone produced in the pineal gland in the brain under dark conditions at night. This interference causes changes in the body's cyclical functions and is what caused the mice to eat at abnormal hours...
Study Finds Possible Link To Obesity
...Childs' discovery has to do with leptin, a hormone that's known to control appetite by acting on specific neurons in the brain. Past studies of leptin have focused on leptin's function within the brain. Childs' study focused on leptin receptors that are on growth hormone cells in the pituitary, which, in addition to stimulating growth of bones and muscle, play a key role in breaking down fat.
In Childs' study, the leptin receptor gene in growth hormone cells was removed in mice. The original purpose was to observe the effects on reproduction, because both leptin and growth hormone are known to be involved in the timing of puberty. However, Childs noticed that whereas puberty was normal, the male mice were becoming overweight as they reached adulthood and the female mice became overweight several months later.
"Tests of serum leptin and leptin receptor levels in the brain suggested that normal leptin is available to effectively control their appetite, and yet they still are gaining weight," Childs said of the genetically altered mice.
She concluded that the obesity was caused by removing the leptin receptor on the mice's growth hormone cells (pituitary somatotropes).
"This is very new; everyone had thought that leptin's most important functions were in the brain to control appetite," she said.
The overweight mice had 60 percent fewer growth hormone cells than the control mice, which means they did not produce enough growth hormone to break down fat as effectively as the control mice. This shows how important leptin is to the maintenance of a normal population of growth hormone cells. It also shows how important growth hormone is to the optimization of body composition including fat...
In Childs' study, the leptin receptor gene in growth hormone cells was removed in mice. The original purpose was to observe the effects on reproduction, because both leptin and growth hormone are known to be involved in the timing of puberty. However, Childs noticed that whereas puberty was normal, the male mice were becoming overweight as they reached adulthood and the female mice became overweight several months later.
"Tests of serum leptin and leptin receptor levels in the brain suggested that normal leptin is available to effectively control their appetite, and yet they still are gaining weight," Childs said of the genetically altered mice.
She concluded that the obesity was caused by removing the leptin receptor on the mice's growth hormone cells (pituitary somatotropes).
"This is very new; everyone had thought that leptin's most important functions were in the brain to control appetite," she said.
The overweight mice had 60 percent fewer growth hormone cells than the control mice, which means they did not produce enough growth hormone to break down fat as effectively as the control mice. This shows how important leptin is to the maintenance of a normal population of growth hormone cells. It also shows how important growth hormone is to the optimization of body composition including fat...
Polluted air 'ups obesity risk in young animals'
A new research showed that exposure to polluted air early in life led to an accumulation of abdominal fat and insulin resistance in mice even if they ate a normal diet.
Animals exposed to the fine-particulate air pollution had larger and more fat cells in their abdominal area and higher blood sugar levels than did animals eating the same diet but breathing clean air.
Researchers exposed the mice to the polluted air for six hours a day, five days a week for 10 weeks beginning when the animals were 3 weeks old. This time frame roughly matches the toddler years to late adolescence in humans...
Animals exposed to the fine-particulate air pollution had larger and more fat cells in their abdominal area and higher blood sugar levels than did animals eating the same diet but breathing clean air.
Researchers exposed the mice to the polluted air for six hours a day, five days a week for 10 weeks beginning when the animals were 3 weeks old. This time frame roughly matches the toddler years to late adolescence in humans...
A couch-potato mouse? Sanford-Burnham researchers say it holds key to obesity
Scientists at Orlando's Sanford-Burnham Medical Research Institute have come up with an unusual new model for studying the way muscles work and how that relates to obesity: a couch-potato mouse.
In a new study being released today in the journal Cell Metabolism, Dr. Daniel Kelly and a team of colleagues at Sanford-Burnham's Lake Nona campus created laboratory mice with very low levels of a protein called PGC-1 in their muscles.
Kelly and his team were surprised to find that the mice they engineered with the low protein levels were not obese or overweight. Instead, they looked normal and walked around without problems.
But put them on a treadmill and they could only run short distances. While the average mouse could last 170 minutes on a treadmill, the couch-potato mouse ran only 6.6 minutes...
In a new study being released today in the journal Cell Metabolism, Dr. Daniel Kelly and a team of colleagues at Sanford-Burnham's Lake Nona campus created laboratory mice with very low levels of a protein called PGC-1 in their muscles.
Kelly and his team were surprised to find that the mice they engineered with the low protein levels were not obese or overweight. Instead, they looked normal and walked around without problems.
But put them on a treadmill and they could only run short distances. While the average mouse could last 170 minutes on a treadmill, the couch-potato mouse ran only 6.6 minutes...
Sunday, November 28, 2010
Fat Yet Muscular Mouse Provides Clues To Improving Cardiovascular Health
A fat yet muscular mouse is helping researchers learn whether more muscle improves the cardiovascular health of obese individuals.
"We are looking for ways to counteract the unhealthy effects of fat," said Dr. David Stepp, vascular biologist at the Medical College of Georgia Vascular Biology Center and co-director of MCG's Diabetes & Obesity Discovery Institute.
Obesity increases the risk for cardiovascular disease as well as diabetes, which essentially doubles the cardiovascular risk. But Stepp's laboratory research indicates more muscle could reduce that risk - a theory bolstered by people who appear "fit and fat." He recently received a $450,000 exploratory grant from the National Institutes of Health to further explore the possibilities.
The fact is that people - and mice - with more muscle have more blood vessels, use more oxygen and energy and eliminate more glucose even sitting still than their flabbier counterparts. "Fat does not consume a lot of energy and it's not very vascular," Stepp said. "Muscle and nerves, on the other hand, generate electricity, which is one of the most energetically expensive things we do." The heart and blood vessels also thrive with increased blood flow and diabetes risk is reduced by muscles' glucose disposal capabilities...
"We are looking for ways to counteract the unhealthy effects of fat," said Dr. David Stepp, vascular biologist at the Medical College of Georgia Vascular Biology Center and co-director of MCG's Diabetes & Obesity Discovery Institute.
Obesity increases the risk for cardiovascular disease as well as diabetes, which essentially doubles the cardiovascular risk. But Stepp's laboratory research indicates more muscle could reduce that risk - a theory bolstered by people who appear "fit and fat." He recently received a $450,000 exploratory grant from the National Institutes of Health to further explore the possibilities.
The fact is that people - and mice - with more muscle have more blood vessels, use more oxygen and energy and eliminate more glucose even sitting still than their flabbier counterparts. "Fat does not consume a lot of energy and it's not very vascular," Stepp said. "Muscle and nerves, on the other hand, generate electricity, which is one of the most energetically expensive things we do." The heart and blood vessels also thrive with increased blood flow and diabetes risk is reduced by muscles' glucose disposal capabilities...
The fat cat cometh
IN THEIR attempts to explain the global epidemic of obesity, researchers have often taken to fingering culprits beyond people’s direct control. It is now believed that increased levels of stress, climate change and even artificial light at night may contribute to expanding waistlines. However, if such factors affect humans, they ought, in principle, to have similarly nefarious effects on other creatures. This should hold especially true for species that are physiologically similar to people and live in proximity to them. Pet owners have long fretted that this may, indeed, be happening.
Of course, anecdotal evidence carries little weight, so a group of researchers led by Yann Klimentidis, of the University of Alabama, decided to check whether animal obesity rates do in fact mirror the worrying trend among people. They published their findings this week in the Proceedings of the Royal Society.
Dr Klimentidis and his team set about their task by scouring online repositories of scientific papers, contacting fellow researchers and even petitioning pet-food companies for data on changes in animals’ bodyweights over the decades. They limited their search to mammals, whose bodies work much like humans’ do—and, specifically, to those mammals living with or around people in the rich world.
The trawl threw up information on more than 20,000 animals from 24 distinct populations covering eight species. These included cats, dogs, mice, rats and several types of monkey. Some were bred in highly controlled research environments. Others lived in people’s homes or in the wild. None had their food intake artificially limited or, as with livestock, ramped up...
Of course, anecdotal evidence carries little weight, so a group of researchers led by Yann Klimentidis, of the University of Alabama, decided to check whether animal obesity rates do in fact mirror the worrying trend among people. They published their findings this week in the Proceedings of the Royal Society.
Dr Klimentidis and his team set about their task by scouring online repositories of scientific papers, contacting fellow researchers and even petitioning pet-food companies for data on changes in animals’ bodyweights over the decades. They limited their search to mammals, whose bodies work much like humans’ do—and, specifically, to those mammals living with or around people in the rich world.
The trawl threw up information on more than 20,000 animals from 24 distinct populations covering eight species. These included cats, dogs, mice, rats and several types of monkey. Some were bred in highly controlled research environments. Others lived in people’s homes or in the wild. None had their food intake artificially limited or, as with livestock, ramped up...
http://www.bionews.org.uk/page_82515.asp
Scientists have found a direct link between the 'fat mass and obesity associated' (Fto) gene and increased weight. Research published in 2007 uncovered an association between variations in the Fto gene and increased body weight in humans.
The Fto gene is not the only gene associated with increased predisposition to obesity, but it is the most significant genetic factor so far identified. Seventeen percent of Europeans have two copies of a common Fto variant. On average, this population is 3kg heavier and has a 1.3 times greater likelihood of being obese.
Until now it was not known whether the link between obesity and Fto was direct or caused by some other factor. The team at MRC Harwell in Oxford predicted that increased expression of Fto may be causing obesity since the Fto variant in humans has been linked to increased expression of the gene in some tissues. To test this, they bred mice with extra copies of the Fto gene.
The team found that the test mice became fatter than the normal mice. What's more, the increase in weight gain was greater the more copies of the gene the test mice had. The researchers attributed the weight gain to an increase in food intake rather than differences in the way the mice metabolise their food...
The Fto gene is not the only gene associated with increased predisposition to obesity, but it is the most significant genetic factor so far identified. Seventeen percent of Europeans have two copies of a common Fto variant. On average, this population is 3kg heavier and has a 1.3 times greater likelihood of being obese.
Until now it was not known whether the link between obesity and Fto was direct or caused by some other factor. The team at MRC Harwell in Oxford predicted that increased expression of Fto may be causing obesity since the Fto variant in humans has been linked to increased expression of the gene in some tissues. To test this, they bred mice with extra copies of the Fto gene.
The team found that the test mice became fatter than the normal mice. What's more, the increase in weight gain was greater the more copies of the gene the test mice had. The researchers attributed the weight gain to an increase in food intake rather than differences in the way the mice metabolise their food...
Sunday, November 21, 2010
Genes 'regulating obesity' in men found
Scientists have found genes that contribute to the risk of obesity in men.
A genome-wide linkage scan for high body mass index (BMI) in 3,893 men and 4,445 women has identified a link on chromosome 5q13-15.
Analysis of this chromosome has revealed a rare cluster of gene types linked to high BMI in men but not women. The portion of the chromosome related to high BMI risk contains a single gene named "arrestin domain containing 3" (Arrdc3).
Researchers investigated Arrdc3 expression and detected it in human fat and muscle. Analysis of gene expression in human abdominal fat biopsies showed significant correlation of Arrdc3 messenger RNA with BMI in men but not women, supporting the male-specific linkage to obesity.
The study also found that fasting increased Arrdc3 expression in both human and mouse fat tissue, suggesting that Arrdc3 functions to conserve energy when food is not available.
To test whether the gene causally regulates obesity, the scientist generated a mouse without Arrdc3. The mice without Arrdc3 showed a "striking resistance" to age-induced obesity: ale mice without Arrdc3 had a smaller total body mass compared to mice with the gene...
A genome-wide linkage scan for high body mass index (BMI) in 3,893 men and 4,445 women has identified a link on chromosome 5q13-15.
Analysis of this chromosome has revealed a rare cluster of gene types linked to high BMI in men but not women. The portion of the chromosome related to high BMI risk contains a single gene named "arrestin domain containing 3" (Arrdc3).
Researchers investigated Arrdc3 expression and detected it in human fat and muscle. Analysis of gene expression in human abdominal fat biopsies showed significant correlation of Arrdc3 messenger RNA with BMI in men but not women, supporting the male-specific linkage to obesity.
The study also found that fasting increased Arrdc3 expression in both human and mouse fat tissue, suggesting that Arrdc3 functions to conserve energy when food is not available.
To test whether the gene causally regulates obesity, the scientist generated a mouse without Arrdc3. The mice without Arrdc3 showed a "striking resistance" to age-induced obesity: ale mice without Arrdc3 had a smaller total body mass compared to mice with the gene...
'Hunger hormone' activating enzyme holds promise as obesity target
Blocking a key gut enzyme involved in the hunger response can reduce weight gain in mice, say US and Taiwanese researchers. The approach could eventually lead to treatments for obesity in humans that would work by damping down hunger pangs.
The market for obesity drugs is worth over $1 billion (£625 million) a year, with some 300 million potential patients. A current focus for drug developers is synthetic hormones that mimic the actions of gut hormones involved in controlling blood sugar levels. Some have already been approved for use in diabetes...
The market for obesity drugs is worth over $1 billion (£625 million) a year, with some 300 million potential patients. A current focus for drug developers is synthetic hormones that mimic the actions of gut hormones involved in controlling blood sugar levels. Some have already been approved for use in diabetes...
'Fat gene' may lead to a thin pill
...People with two copies of the genetic variant – about 16 per cent of all Europeans – were on average 3kg (6.6lbs) heavier than those without it.
In this latest study, scientists bred mice with extra copies of the FTO gene. They found that the test mice, although healthy, ate more and became fatter than normal mice.
Prof Frances Ashcroft, one of the leaders of the research, said: "This work makes us confident that FTO is an important gene that contributes to obesity.
"We can now think about developing drugs that turn down the activity of the FTO gene as potential anti-obesity pills. That's a long way off and there's no certainty of success, but it's an enticing prospect."...
In this latest study, scientists bred mice with extra copies of the FTO gene. They found that the test mice, although healthy, ate more and became fatter than normal mice.
Prof Frances Ashcroft, one of the leaders of the research, said: "This work makes us confident that FTO is an important gene that contributes to obesity.
"We can now think about developing drugs that turn down the activity of the FTO gene as potential anti-obesity pills. That's a long way off and there's no certainty of success, but it's an enticing prospect."...
Monday, November 08, 2010
Born to be fat
...Studies on animals have shown that exposure around the time of birth to even trace amounts of everyday chemicals can predispose subjects to weight gain throughout life. Perfluorooctanoic acid, found in non-stick pans, microwave popcorn bags and pizza boxes, has been associated with obesity in female mice. Bisphenol A, used in plastics and recently declared a toxic chemical in Canada, is linked to obesity in rats. Similarly, triclosan, an ingredient in antibacterial hand soaps, dishwashing detergents and other body care products, has been correlated to faster growth in frogs. Caren Helbing, a researcher at the University of Victoria who worked on the triclosan study, notes, “It’s critical to realize that some of the manufactured chemicals that have been important for protecting people, like flame retardants, were designed without thinking about how they would change the way hormones in humans work.”
The grandfather of the obesogen studies is Bruce Blumberg, a cell biologist at the University of California, Irvine. He coined the term “obesogen,” and has focused on mice and how they are affected by tributyltin (TBT), a pesticide added to paint used on ships to prevent the growth of marine organisms like barnacles and algae, which enters underwater environments and ends up in our seafood. “We found that if we treat pregnant mice with tributyltin, the pups in their womb will be predisposed to getting fat later in life,” Blumberg says. “They make more fat cells, and that appears to lead them to be heavier.”..
The grandfather of the obesogen studies is Bruce Blumberg, a cell biologist at the University of California, Irvine. He coined the term “obesogen,” and has focused on mice and how they are affected by tributyltin (TBT), a pesticide added to paint used on ships to prevent the growth of marine organisms like barnacles and algae, which enters underwater environments and ends up in our seafood. “We found that if we treat pregnant mice with tributyltin, the pups in their womb will be predisposed to getting fat later in life,” Blumberg says. “They make more fat cells, and that appears to lead them to be heavier.”..
Saturday, November 06, 2010
Gastric Bypass Alters Sweet Taste Function
Gastric bypass surgery decreases the preference for sweet-tasting substances in obese rats, a study finding that could help in developing safer treatments for the morbidly obese, according to Penn State College of Medicine researchers.
"Roux-en-Y gastric bypass surgery is the most common effective treatment for morbid obesity," said Andras Hajnal, M.D., Ph.D., associate professor, Department of Neural and Behavioral Science and Surgery. "Many patients report altered taste preferences after having the procedure."
This surgery involves the creation of a small gastric pouch and bypassing a portion of the upper small intestine. Unlike other weight-reduction methods, it produces substantial and durable weight loss and significant improvements in obesity-related medical conditions including diabetes.
Study results in obese rats suggest that post-surgery changes in the gastrointestinal anatomy affect change in the brain that relate to taste...
"Roux-en-Y gastric bypass surgery is the most common effective treatment for morbid obesity," said Andras Hajnal, M.D., Ph.D., associate professor, Department of Neural and Behavioral Science and Surgery. "Many patients report altered taste preferences after having the procedure."
This surgery involves the creation of a small gastric pouch and bypassing a portion of the upper small intestine. Unlike other weight-reduction methods, it produces substantial and durable weight loss and significant improvements in obesity-related medical conditions including diabetes.
Study results in obese rats suggest that post-surgery changes in the gastrointestinal anatomy affect change in the brain that relate to taste...
Sunday, October 31, 2010
Biochemical Approach to Treating Diabetes May Replace Diabetes Drugs
A surprise discovery of a protein that helps regulate glucose may be especially good news for shift workers, and could lead to new ways of treating obesity and diabetes.
Online PR News – 27-October-2010 – Biologists experimenting with mice have uncovered a possible new biological approach to treating obesity and type 2 diabetes. Their work also raises some interesting questions about the role disturbances in the human sleep cycle plays in the rise of diabetes in the US and other industrialized countries...
Online PR News – 27-October-2010 – Biologists experimenting with mice have uncovered a possible new biological approach to treating obesity and type 2 diabetes. Their work also raises some interesting questions about the role disturbances in the human sleep cycle plays in the rise of diabetes in the US and other industrialized countries...
OSU study links light exposure to obesity in mice
A recent Ohio State study found that eight weeks of exposure to light at night caused mice to gain nearly 50 percent more weight than mice given eight hours of darkness daily...
Sunday, October 24, 2010
Study says sitting down changes our body chemistry
If you're sitting down you may want to get up and take a walk around. A new study says that sitting actually changes our bed (sic) chemistry, affecting how long we live. Researchers found that when lab mice were prevented from running around they put on weight. Being sedentary turns off an important chemical that burns fat.
People sitting longer than six hours a day are more likely to die from diabetes, heart disease and obesity. Men are 18% more likely, women are 37%.
People sitting longer than six hours a day are more likely to die from diabetes, heart disease and obesity. Men are 18% more likely, women are 37%.
Gluttonous Male Mice Give Diabetes to Daughters
A prospective dad’s diet may affect the health of his future children, suggests a study of cross-generational nutritional impacts in mice.
Males were fed a high-fat diet, becoming obese and diabetic, then mated with lean, healthy females. At six weeks of age, or the mouse equivalent of puberty, their daughters became glucose-intolerant, a major step toward diabetes.
That overweight moms are more likely to have overweight babies is known, but the phenomenon hadn’t before been demonstrated in males of any species...
Males were fed a high-fat diet, becoming obese and diabetic, then mated with lean, healthy females. At six weeks of age, or the mouse equivalent of puberty, their daughters became glucose-intolerant, a major step toward diabetes.
That overweight moms are more likely to have overweight babies is known, but the phenomenon hadn’t before been demonstrated in males of any species...
Shining a Night Light on Obesity
f you're wishing upon a star in hopes to stop packing on the pounds, you might already be jinxing yourself. A recent study finds that continual exposure to light at night may lead to weight gain, even without changing physical activity or eating more food. Researchers say that instead of wishing upon the stars . . . maybe you should sleep under them.
Researchers found that mice that were exposed to a moderately dim light at night over eight weeks had a body mass that was around 50 percent more than other mice that lived in a standard light-dark cycle. "Although there were no differences in activity levels or daily consumption of food, the mice that lived with light at night were getting fatter than the others," which Laura Fonken, lead author of the study and a doctoral student in neuroscience at Ohio State University, was quoted as saying.
The study revealed that the mice living with light at night eat at times they normally wouldn't, which is a main factor of their weight gain. One study showed that mice exposed to light at night -- but with food restricted to normal eating times -- gained no more weight than did mice in a normal light-dark cycle.
"Something about light at night was making the mice in our study want to eat at the wrong times to properly metabolize their food," which Randy Nelson, co-author of the study and professor of neuroscience and psychology at Ohio State, was quoted as saying. If these results are confirmed in humans, it would verify that late-night snacking is a possible risk factor for obesity.
In another study, mice were housed in one of three condition: 24 hours of constant light, a standard light-dark cycle (16 hours of light at 150 lux, 8 hours of dark), or 16 hours of daylight and 8 hours of dim light (approximately 5 lux of light).
Researchers measured the amount of food the mice ate each day, in addition to how much they moved in their cages each day using an infrared beam crossing system. Furthermore, body mass was calculated each week. Compared to mice in the standard dark-light cycle, mice that were exposed to dim light at night showed notably higher increases in body mass, beginning in the commencement of the study and continuing to end.
Light-at-night mice had gained 12 grams of body mass by the end of the experiment, compared to 8 grams for those in the standard light-dark cycle. It was reported that mice in constant bright light additionally gained more than those in the standard light-dark cycle; however the scientists stated that the dim light-at-night mice were better comparisons to the light exposure human generally are exposed to.
What's more, the dim light-at-night mice showed higher levels of epididymal fat as well as impaired glucose tolerance - a marker for pre-diabetes...
Researchers found that mice that were exposed to a moderately dim light at night over eight weeks had a body mass that was around 50 percent more than other mice that lived in a standard light-dark cycle. "Although there were no differences in activity levels or daily consumption of food, the mice that lived with light at night were getting fatter than the others," which Laura Fonken, lead author of the study and a doctoral student in neuroscience at Ohio State University, was quoted as saying.
The study revealed that the mice living with light at night eat at times they normally wouldn't, which is a main factor of their weight gain. One study showed that mice exposed to light at night -- but with food restricted to normal eating times -- gained no more weight than did mice in a normal light-dark cycle.
"Something about light at night was making the mice in our study want to eat at the wrong times to properly metabolize their food," which Randy Nelson, co-author of the study and professor of neuroscience and psychology at Ohio State, was quoted as saying. If these results are confirmed in humans, it would verify that late-night snacking is a possible risk factor for obesity.
In another study, mice were housed in one of three condition: 24 hours of constant light, a standard light-dark cycle (16 hours of light at 150 lux, 8 hours of dark), or 16 hours of daylight and 8 hours of dim light (approximately 5 lux of light).
Researchers measured the amount of food the mice ate each day, in addition to how much they moved in their cages each day using an infrared beam crossing system. Furthermore, body mass was calculated each week. Compared to mice in the standard dark-light cycle, mice that were exposed to dim light at night showed notably higher increases in body mass, beginning in the commencement of the study and continuing to end.
Light-at-night mice had gained 12 grams of body mass by the end of the experiment, compared to 8 grams for those in the standard light-dark cycle. It was reported that mice in constant bright light additionally gained more than those in the standard light-dark cycle; however the scientists stated that the dim light-at-night mice were better comparisons to the light exposure human generally are exposed to.
What's more, the dim light-at-night mice showed higher levels of epididymal fat as well as impaired glucose tolerance - a marker for pre-diabetes...
Tuesday, October 19, 2010
Obesity therapy gains as test rats don’t overeat
One of the more offbeat ideas in the business of developing drugs to treat obesity has some new evidence behind it.
Boston-based Gelesis, the developer of a super-absorbent capsule designed to swell up in the stomach and make people feel full, said its treatment was able to help rats reduce their food intake over 18 hours. The findings were presented at the Obesity Society’s recent annual meeting in San Diego.
While it’s too early to say the treatment will work in people, many other weight-loss drugs have been tripped up by safety concerns. But the rat study is interesting, in part, because it comes about six months after Gelesis reported on a more rigorous clinical trial of 95 patients. The other study showed that the capsules helped people feel full after meals and less hungry in between...
Boston-based Gelesis, the developer of a super-absorbent capsule designed to swell up in the stomach and make people feel full, said its treatment was able to help rats reduce their food intake over 18 hours. The findings were presented at the Obesity Society’s recent annual meeting in San Diego.
While it’s too early to say the treatment will work in people, many other weight-loss drugs have been tripped up by safety concerns. But the rat study is interesting, in part, because it comes about six months after Gelesis reported on a more rigorous clinical trial of 95 patients. The other study showed that the capsules helped people feel full after meals and less hungry in between...
Sunday, October 17, 2010
Phospholipid shows anti-obesity potential, in mice at least
Supplementation of the diet with the phospholipid phosphatidylinositol may exert an anti-obesity effect by modifying gene expression in the liver, suggests a new study with mice.
If the findings, published in the Journal of Agricultural and Food Chemistry, can be repeated in further studies, it could see phosphatidylinositol established as an ingredient with potential weight management potential...
If the findings, published in the Journal of Agricultural and Food Chemistry, can be repeated in further studies, it could see phosphatidylinositol established as an ingredient with potential weight management potential...
Nighttime Light Ups Weight in Mice
The gentle glow of the television at night may be contributing to the obesity epidemic, findings from a mouse study suggest.
Mice exposed to even dim light at night gained significantly more weight and lost glucose tolerance compared with mice housed in a dark environment at night, Laura K. Fonken, a graduate student at Ohio State University, in Columbus, and colleagues found.
The night light-exposed mice didn't eat more or move around less overall, but did shift to more munching at off hours when they were inactive...
Mice exposed to even dim light at night gained significantly more weight and lost glucose tolerance compared with mice housed in a dark environment at night, Laura K. Fonken, a graduate student at Ohio State University, in Columbus, and colleagues found.
The night light-exposed mice didn't eat more or move around less overall, but did shift to more munching at off hours when they were inactive...
Sunday, October 10, 2010
Getting to the bottom of diabetes and kidney disease
Diabetic kidney disease may result as much from a failure of certain renal cells to access insulin as it does from runaway blood sugar, a new study shows. The findings in mice suggests that targeting the condition known as insulin resistance might protect the kidneys of people with diabetes, researchers report in the October Cell Metabolism.
Fully half of all kidney disease that leads to dialysis or a transplant occurs in people with diabetes, and most have the common type 2 form that typically shows up in adulthood. Type 2 diabetes has clear links to obesity, lack of exercise and insulin resistance in which cells fail to capture glucose efficiently from the bloodstream after digestion of food. While the precise cause of insulin resistance remains unclear, there’s no question it starves cells, forces the pancreas to work overtime making more insulin and leaves a person with high blood sugar...
Fully half of all kidney disease that leads to dialysis or a transplant occurs in people with diabetes, and most have the common type 2 form that typically shows up in adulthood. Type 2 diabetes has clear links to obesity, lack of exercise and insulin resistance in which cells fail to capture glucose efficiently from the bloodstream after digestion of food. While the precise cause of insulin resistance remains unclear, there’s no question it starves cells, forces the pancreas to work overtime making more insulin and leaves a person with high blood sugar...
Video feature: Developing a treatment for obesity based on natural appetite suppression
Over 30 000 deaths a year are caused by obesity in England alone and yet the need for safe and effective anti-obesity therapies is largely unmet. With funding from the Wellcome Trust's Seeding Drug Discovery initiative in 2007, Professor Bloom and his team have developed a novel, synthetic form of pancreatic polypeptide that can cause a significant reduction in food intake and body weight in mice. The lead compound, PP1420, entered phase I clinical trials in mid2010. If successful, the proposed research may lead to a treatment within five - eight years.
Saturday, October 02, 2010
Blueberries Help Fight Artery Hardening, Lab Animal Study Indicates
Blueberries may help fight atherosclerosis, also known as hardening of the arteries, according to results of a preliminary U.S. Department of Agriculture (USDA)-funded study with laboratory mice. The research provides the first direct evidence that blueberries can help prevent harmful plaques or lesions, symptomatic of atherosclerosis, from increasing in size in arteries...
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