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...
Thursday, May 26, 2011
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...
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