Researchers at the University of Porto in Portugal have developed a vaccine that fights obesity by suppressing the hormone ghrelin, which is an appetite stimulant.
“An anti-ghrelin vaccine may become an alternate treatment for obesity, to be used in combination with diet and exercise,” said lead investigator Dr. Mariana Monteiro. In other words, this vaccine may someday be a viable alternative to weight loss surgery.
The vaccine, which was developed through the observation of its effects on lab rats, showed a decrease in food consumption and an increase in calorie burning in mice that received the treatment. The suppression of ghrelin, a hormone found in the gut, can lessen appetite while boosting metabolism, promoting weight loss. Weight loss surgery, such as gastric bypass surgery, also suppresses ghrelin. This can, in part, explain the successful weight loss that most patients experience after having obesity surgery.
Lab mice that were given the vaccine also showed decreased levels of neuropeptide Y (NPY), which is responsible for increasing the appetite signals in the central nervous system...
Wednesday, June 22, 2011
Obesity: Cysteine Plays a Key Role: Amino Acid May Be at Root of Obesity
People with high levels of the amino acid cysteine carry 6-10 kilograms more fat than other people. Norwegian researchers studying this phenomenon are generating knowledge which could help to prevent and treat life-threatening obesity.
"There is a very high correlation between high levels of cysteine and obesity," explains Professor of Nutrition Helga Refsum of the University of Oslo's Department of Nutrition. The question is whether this is a causal relationship. Is much of the body's fat due to a high cysteine level, and if so, what is the connection? Why do some people have higher cysteine levels than others? How much is owing to genetic factors, and how much is affected by diet?
Researchers are now closing in on some answers. A comprehensive study, funded under the Research Council of Norway's funding scheme for independent basic research (FRIPRO), aims to shed light on the underlying biological mechanism linking cysteine to obesity. The project started up in 2010 and will run until 2013.
Cooperation between Oslo and Oxford
As an outstanding young researcher in Norway in 1998, Helga Refsum was awarded a grant which she used to build up a working relationship with Oxford University and Dr. Amany Elshorbagy. Their collaboration led to the discovery of a connection between cysteine and obesity.
The project has evolved into a close collaboration between the University of Oslo and Oxford University, involving several other research institutions as well.
Affects more than weight
Obesity is caused by the intake of more calories than are burned; any surplus is stored as fat in the body. The concept is a simple one at the general level. But at the molecular level, many more facets to this relationship emerge, making it more difficult to pin down. The long, complex biochemical processes of enzymes converting food to energy and building blocks can be affected by many factors. The same is true for the breakdown of fat.
Professor Refsum's research indicates that cysteine plays a key role in how the body metabolises energy, stores fat, and breaks down fat. In this latest project, the researchers will also study how cysteine affects the brain -- for instance, whether cysteine can influence the feeling of being satiated.
Blame our genes
Our genes play a large part in determining our weight.
"We know there is a strong genetic component to the body's weight and fat content," says Professor Refsum, pointing out that 50-80 per cent of body weight is due to genetic factors. "Look at the difference between males and females! Women always have more body fat than men. Nature intended it this way; this is how it should be."
Body fat percentage varies widely between ethnic groups. Taking these differences into account, health personnel tailor their body mass index (BMI) criteria for obesity to different populations.
Genetic factors are undoubtedly involved in cysteine levels, the professor stresses. Indeed, two known genetic conditions demonstrate a clear relationship.
People with the most common form of a genetic condition known as homocystinuria lack one of the enzymes that convert homocysteine to cysteine. These people have low cysteine levels and are extremely slender. By contrast, people with a different genetic condition, Down's syndrome, have 50% more of that same enzyme than normal- and they also have higher-than-average cysteine levels and tend to be overweight.
Public health focus
The connection between cysteine and obesity-related diseases is a major topic of Professor Refsum's research.
"We particularly want to find out if cysteine is associated with obesity-related morbidity -- the myriad of diseases such as diabetes, cardiovascular diseases and certain types of cancer that are associated with obesity. From a public health perspective, it is this aspect of obesity we need to worry about.
With lowered cysteine, mice shed fat
Professor Refsum and her colleagues have demonstrated that reducing cysteine levels leads to weight loss in mice and rats. With subsequent supplements of cysteine, the weight returns -- along with a higher risk of diabetes...
"There is a very high correlation between high levels of cysteine and obesity," explains Professor of Nutrition Helga Refsum of the University of Oslo's Department of Nutrition. The question is whether this is a causal relationship. Is much of the body's fat due to a high cysteine level, and if so, what is the connection? Why do some people have higher cysteine levels than others? How much is owing to genetic factors, and how much is affected by diet?
Researchers are now closing in on some answers. A comprehensive study, funded under the Research Council of Norway's funding scheme for independent basic research (FRIPRO), aims to shed light on the underlying biological mechanism linking cysteine to obesity. The project started up in 2010 and will run until 2013.
Cooperation between Oslo and Oxford
As an outstanding young researcher in Norway in 1998, Helga Refsum was awarded a grant which she used to build up a working relationship with Oxford University and Dr. Amany Elshorbagy. Their collaboration led to the discovery of a connection between cysteine and obesity.
The project has evolved into a close collaboration between the University of Oslo and Oxford University, involving several other research institutions as well.
Affects more than weight
Obesity is caused by the intake of more calories than are burned; any surplus is stored as fat in the body. The concept is a simple one at the general level. But at the molecular level, many more facets to this relationship emerge, making it more difficult to pin down. The long, complex biochemical processes of enzymes converting food to energy and building blocks can be affected by many factors. The same is true for the breakdown of fat.
Professor Refsum's research indicates that cysteine plays a key role in how the body metabolises energy, stores fat, and breaks down fat. In this latest project, the researchers will also study how cysteine affects the brain -- for instance, whether cysteine can influence the feeling of being satiated.
Blame our genes
Our genes play a large part in determining our weight.
"We know there is a strong genetic component to the body's weight and fat content," says Professor Refsum, pointing out that 50-80 per cent of body weight is due to genetic factors. "Look at the difference between males and females! Women always have more body fat than men. Nature intended it this way; this is how it should be."
Body fat percentage varies widely between ethnic groups. Taking these differences into account, health personnel tailor their body mass index (BMI) criteria for obesity to different populations.
Genetic factors are undoubtedly involved in cysteine levels, the professor stresses. Indeed, two known genetic conditions demonstrate a clear relationship.
People with the most common form of a genetic condition known as homocystinuria lack one of the enzymes that convert homocysteine to cysteine. These people have low cysteine levels and are extremely slender. By contrast, people with a different genetic condition, Down's syndrome, have 50% more of that same enzyme than normal- and they also have higher-than-average cysteine levels and tend to be overweight.
Public health focus
The connection between cysteine and obesity-related diseases is a major topic of Professor Refsum's research.
"We particularly want to find out if cysteine is associated with obesity-related morbidity -- the myriad of diseases such as diabetes, cardiovascular diseases and certain types of cancer that are associated with obesity. From a public health perspective, it is this aspect of obesity we need to worry about.
With lowered cysteine, mice shed fat
Professor Refsum and her colleagues have demonstrated that reducing cysteine levels leads to weight loss in mice and rats. With subsequent supplements of cysteine, the weight returns -- along with a higher risk of diabetes...
Nicotine: A cure for obesity?
Many cigarette smokers have shed extra pounds through their otherwise-unhealthy nicotine habit. But now, scientists have identified and isolated the pathways in the brain that are affected by nicotine's appetite suppressants. The research, published in the journal Science, might lead to the development of a healthy, nicotine-based treatment to control obesity. Here, a short guide to the findings:
How did the researchers make their discovery?
It was accidental, actually. Researchers from Yale and Baylor were looking for new drugs to treat depression, when they noticed that mice given nicotine were eating less. The scientists gave the mice a chemical compound that blocked nicotine receptors, and the rodents' appetites returned. Next, the researchers genetically modified some mice to knock out those nicotine receptors. When given nicotine, the mice without nicotine receptors did not lose weight, but mice with the receptors did. The researchers also found that these receptors are independent from those known to trigger tobacco cravings in smokers...
How did the researchers make their discovery?
It was accidental, actually. Researchers from Yale and Baylor were looking for new drugs to treat depression, when they noticed that mice given nicotine were eating less. The scientists gave the mice a chemical compound that blocked nicotine receptors, and the rodents' appetites returned. Next, the researchers genetically modified some mice to knock out those nicotine receptors. When given nicotine, the mice without nicotine receptors did not lose weight, but mice with the receptors did. The researchers also found that these receptors are independent from those known to trigger tobacco cravings in smokers...
Fat affects brain's ability to control weight: study
The relationship between a high-fat diet and obesity may be more complicated than was previously thought, according to a new study unveiled at the annual meeting of the Endocrine Society in Boston.
Eating fatty foods may injure neurons in an area of the brain that controls body weight, found researchers at the Diabetes and Obesity Center of Excellence at the University of Washington in Seattle.
"The possibility that brain injury may be a consequence of the overconsumption of a typical American diet offers a new explanation for why sustained weight loss is so difficult for most obese individuals to achieve," said presenting author Joshua Thaler.
Researchers studied rats and mice fed a high-fat diet - that is, one with a similar fat content to the average American diet - for periods varying between one day and eight months. A detailed analysis was then carried out on the animals' brains.
Within the first three days on the diet, the rodents were consuming nearly double the daily calories that they usually would...
Eating fatty foods may injure neurons in an area of the brain that controls body weight, found researchers at the Diabetes and Obesity Center of Excellence at the University of Washington in Seattle.
"The possibility that brain injury may be a consequence of the overconsumption of a typical American diet offers a new explanation for why sustained weight loss is so difficult for most obese individuals to achieve," said presenting author Joshua Thaler.
Researchers studied rats and mice fed a high-fat diet - that is, one with a similar fat content to the average American diet - for periods varying between one day and eight months. A detailed analysis was then carried out on the animals' brains.
Within the first three days on the diet, the rodents were consuming nearly double the daily calories that they usually would...
Sunday, June 12, 2011
The RNA roots of obesity?
Two upregulated microRNA molecules may lie at the heart of insulin signalling malfunctions, which can lead to obesity and type 2 diabetes, according to researchers in Switzerland. Scientists at ETH Zurich found that silencing the two microRNAs improved glucose sensitivity in obese mice, and in a paper published today (8 June) in Nature, they suggest that the findings may point the way to potential obesity treatments in humans.
“The effects they are showing are quite striking,” said Phillip Scherer, a fat cell physiologist at the University of Texas Southwestern Medical School, who was not involved in the study. The microRNAs studied in the paper were “so blatantly, obviously up-regulated in the obese state.”...
“The effects they are showing are quite striking,” said Phillip Scherer, a fat cell physiologist at the University of Texas Southwestern Medical School, who was not involved in the study. The microRNAs studied in the paper were “so blatantly, obviously up-regulated in the obese state.”...
Yo-Yo Dieting Healthier Than Obesity?
In a recent study comparing lifelong obesity to the weight fluctuations of "yo-yo dieting," it is suggested that it’s better to attempt to lose weight than to not diet and stay obese.
"It is clear that remaining on a stable, healthy diet provides the best outcome for health and longevity," which the study's principal investigator, Edward List, PhD, a scientist at Ohio University, Athens, was quoted as saying.
"However, obese individuals commonly weight cycle — they have repeated intentional weight loss followed by weight regain, often called yo-yo dieting. While yo-yo dieting is thought to be harmful, there is little hard scientific evidence to support that."
In order to verify the long-term health effects of yo-yo dieting, List and his collaborators performed what they call "the first controlled study of a yo-yo diet regimen used for an entire life span" with the aid of mice...
"It is clear that remaining on a stable, healthy diet provides the best outcome for health and longevity," which the study's principal investigator, Edward List, PhD, a scientist at Ohio University, Athens, was quoted as saying.
"However, obese individuals commonly weight cycle — they have repeated intentional weight loss followed by weight regain, often called yo-yo dieting. While yo-yo dieting is thought to be harmful, there is little hard scientific evidence to support that."
In order to verify the long-term health effects of yo-yo dieting, List and his collaborators performed what they call "the first controlled study of a yo-yo diet regimen used for an entire life span" with the aid of mice...
Study links insulin action on brain's reward circuitry to obesity
Researchers reporting in the June issue of Cell Metabolism, a Cell Press publication, have what they say is some of the first solid proof that insulin has direct effects on the reward circuitry of the brain. Mice whose reward centers can no longer respond to insulin eat more and become obese, they show.
The findings suggest that insulin resistance might help to explain why those who are obese may find it so difficult to resist the temptation of food and take the weight back off...
The findings suggest that insulin resistance might help to explain why those who are obese may find it so difficult to resist the temptation of food and take the weight back off...
Anti-obesity vaccine boosts calorie expenditure, curbs appetite in mice
Diet and exercise that are mainstays for treating and preventing obesity might get a boost from a newly developed anti-obesity vaccine found to curb appetite and boost calorie burning in mice...
Nicotine treatment 'could control obesity'
Scientists have identified a group of neurons in the brain responsible for smokers' lack of appetite.
In an article in the journal Science, Yale University researchers describe experiments on mice which found nicotine activates neurons to send signals the body has had enough to eat.
However they are not the same neurons which trigger a craving for tobacco.
As a result, the researchers say nicotine-based treatments could help control obesity.
A research team from Yale University School of Medicine and Baylor College of Medicine in Houston performed a combination of molecular, pharmacological, behavioural and genetic experiments on mice.
They found that nicotine influences a collection of central nervous system circuits, known as the body's hypothalamic melanocortin system, by activating certain receptors.
These receptors, in turn, increase the activity of pro-opiomelanocortin (POMC) neurons, known for their effects on obesity in humans and animals.
Targeting cells
When subjected to nicotine, mice lacking the POMC pathway did not lose weight, but mice with the pathway did...
In an article in the journal Science, Yale University researchers describe experiments on mice which found nicotine activates neurons to send signals the body has had enough to eat.
However they are not the same neurons which trigger a craving for tobacco.
As a result, the researchers say nicotine-based treatments could help control obesity.
A research team from Yale University School of Medicine and Baylor College of Medicine in Houston performed a combination of molecular, pharmacological, behavioural and genetic experiments on mice.
They found that nicotine influences a collection of central nervous system circuits, known as the body's hypothalamic melanocortin system, by activating certain receptors.
These receptors, in turn, increase the activity of pro-opiomelanocortin (POMC) neurons, known for their effects on obesity in humans and animals.
Targeting cells
When subjected to nicotine, mice lacking the POMC pathway did not lose weight, but mice with the pathway did...
Wednesday, June 08, 2011
Adding Tangerines to Your Weight Loss Diet Plan
A recent study based out of the University of Ontario has found that a certain substance found in tangerines has been crucial in preventing obesity in mice. Not only that, but it also helped to protect them from Type 2 Diabetes, another disease also associated with obesity...
Thursday, May 26, 2011
Weight Gain – Brain Protein Found To Contribute To Obesity
Weizmann Institute scientists have added another piece to the obesity puzzle, showing how and why a certain protein that is active in a small part of the brain contributes to weight gain. This research appeared today in Cell Metabolism.
Prof. Ari Elson and his team in the Institute’s Molecular Genetics Department made the discovery when working with female mice that were genetically engineered to lack this protein, called protein tyrosine phosphatase epsilon (PTPe, for short). The scientists had originally intended to investigate osteoporosis, and thus, they also removed the ovaries of these mice. Taking out ovaries typically causes mice to gain weight to the point of obesity – so the scientists were surprised to find that the weight of the genetically-engineered mice remained stable. Working with Dr. Alon Chen and his group in the Neurobiology Department and Prof. Hilla Knobler, Head of the Unit of Metabolic Disease and Diabetes of Kaplan Medical Center, the researchers fed these mice a high-fat diet, yet the PTPe-deficient mice maintained their svelte figures; they burned more energy and had more stable glucose levels as well.
To find out how the lack of this protein could keep mice slim and healthy, the scientists looked at the hypothalamus, a region of the brain that takes in assorted stimuli, including a wide variety of hormones, and sends out messages of its own in the form of new hormones and nerve signals. The hypothalamus plays a vital role in regulating body mass – a complex balancing act that involves, among other things, controlling appetite and physical activity...
Prof. Ari Elson and his team in the Institute’s Molecular Genetics Department made the discovery when working with female mice that were genetically engineered to lack this protein, called protein tyrosine phosphatase epsilon (PTPe, for short). The scientists had originally intended to investigate osteoporosis, and thus, they also removed the ovaries of these mice. Taking out ovaries typically causes mice to gain weight to the point of obesity – so the scientists were surprised to find that the weight of the genetically-engineered mice remained stable. Working with Dr. Alon Chen and his group in the Neurobiology Department and Prof. Hilla Knobler, Head of the Unit of Metabolic Disease and Diabetes of Kaplan Medical Center, the researchers fed these mice a high-fat diet, yet the PTPe-deficient mice maintained their svelte figures; they burned more energy and had more stable glucose levels as well.
To find out how the lack of this protein could keep mice slim and healthy, the scientists looked at the hypothalamus, a region of the brain that takes in assorted stimuli, including a wide variety of hormones, and sends out messages of its own in the form of new hormones and nerve signals. The hypothalamus plays a vital role in regulating body mass – a complex balancing act that involves, among other things, controlling appetite and physical activity...
Mice to reveal key to human obesity
Call him fatso, if you will. And call her a lazy lump if that is what you wish. But the big fat mice and their ilk which live in an exclusive `colony of mice' at a laboratory at Tarnaka will soon reveal to the world what makes them so obese. And here's why what they reveal will be important for the world.
After 14 years of research, scientists at the National Centre for Laboratory Animal Sciences (NCLAS) at the National Insitute of Nutrition (NIN) at Tarnaka are on the verge of a major breakthrough in detecting what makes the experimental breed of mice obese.
The breakthrough will be significant for the world as it will help fight obesity in human beings. Further studies based on the findings in the obese mice will reveal what makes human beings also obese. Obesity is enemy no. 1 in human beings and most diseases are directly related to the problem.
After 14 years of research, scientists at the National Centre for Laboratory Animal Sciences (NCLAS) at the National Insitute of Nutrition (NIN) at Tarnaka are on the verge of a major breakthrough in detecting what makes the experimental breed of mice obese.
The breakthrough will be significant for the world as it will help fight obesity in human beings. Further studies based on the findings in the obese mice will reveal what makes human beings also obese. Obesity is enemy no. 1 in human beings and most diseases are directly related to the problem.
Sunday, May 08, 2011
Silencing a protein could turn fat cells into energy burners in individuals at risk for type 2 diabetes
Silencing the neuropeptide Y (NPY) protein in the brain may turn adipose tissue into a type of fat that burns excess energy rather than storing it, according to a new study from Johns Hopkins University researchers. The findings could have major implications for obese individuals who are at risk for developing type 2 diabetes.
Most adipose tissue in the body is known as white fat. This material is what the body uses to store excess energy and is typically located around the midsection. High levels of this fat have been shown to increase an individual’s risk of chronic diseases, such as heart disease and type 2 diabetes.
However, there is another type of adipose tissue that serves a very different function. Brown fat instructs the body to burn unneeded calories. Most adults have very little of this tissue.
Yet it may be possible for individuals to develop more. The researchers reported in the journal Cell Metabolism that silencing the NPY protein in the brain turns typical white fat cells into energy-burning brown adipose tissue.
The team began experimenting with switching off the expression of NPY protein in laboratory mice because it had previously been shown to mediate feelings of hunger and thirst. They speculated that by silencing the protein, mice would want to eat less. As expected, their study showed that this was the case. However, more surprisingly, mice that lacked expression of the NPY protein also had considerably more brown fat...
Most adipose tissue in the body is known as white fat. This material is what the body uses to store excess energy and is typically located around the midsection. High levels of this fat have been shown to increase an individual’s risk of chronic diseases, such as heart disease and type 2 diabetes.
However, there is another type of adipose tissue that serves a very different function. Brown fat instructs the body to burn unneeded calories. Most adults have very little of this tissue.
Yet it may be possible for individuals to develop more. The researchers reported in the journal Cell Metabolism that silencing the NPY protein in the brain turns typical white fat cells into energy-burning brown adipose tissue.
The team began experimenting with switching off the expression of NPY protein in laboratory mice because it had previously been shown to mediate feelings of hunger and thirst. They speculated that by silencing the protein, mice would want to eat less. As expected, their study showed that this was the case. However, more surprisingly, mice that lacked expression of the NPY protein also had considerably more brown fat...
Researchers Suggest Role for Hypothalamic PPAR-Gamma in Diabetes Drug-Related Weight Gain
Two separate research teams claim that activity of nuclear receptor peroxisome proliferator-activated receptor-γ (PPAR-γ) in the brain plays a role in the mechanisms that cause weight gain among patients receiving thiazolidinedione (TZD) treatment for type 2 diabetes. The two sets of animal-based research, one led by a team at the University of California, San Diego (UCSD), and the other carried out by scientists at the University of Cincinnati College of Medicine, have identified a previously unknown role for central nervous system PPAR-γ in the regulation of energy balance, leptin sensitivity, and at least some of the weight gain associated with administering PPAR-γ–modulating drugs. Both research teams published their results in Nature Medicine...
To investigate this possibility further, Jerrold M. Olefsky, Ph.D., at UCSD’s Department of Medicine, and colleagues, generated mice in which the gene for PPAR-γ was knocked out only in the brain (Pparg brain knockout [BKO] mice), to determine whether neuronal PPAR-γ signalling contributes to either weight gain or insulin sensitivity...
Studies by Dr. Seeley’s team also concurred with those of the UCSD team with regard to the effects of CNS PPAR-γ on leptin signalling. Leptin signalling in the hypothalamus is blunted in rats fed a HFD, and this leptin resistance is thought to contribute to the continued accumulation of body fat. The Cincinnati team hypothesized that hypothalamic PPAR-γ specifically may contribute to the development of HFD-induced leptin resistance, and that chronic antagonism of CNS PPAR-γ would restore leptin sensitivity these animals. To test this, they administered the PPAR-γ antagonist into the lateral ventricle of HFD-fed rats, at a dose that had no effect on body weight but that did result in significantly lower hypothalamic expression of PPAR-γ’s target gene lipoprotein lipase...
To investigate this possibility further, Jerrold M. Olefsky, Ph.D., at UCSD’s Department of Medicine, and colleagues, generated mice in which the gene for PPAR-γ was knocked out only in the brain (Pparg brain knockout [BKO] mice), to determine whether neuronal PPAR-γ signalling contributes to either weight gain or insulin sensitivity...
Studies by Dr. Seeley’s team also concurred with those of the UCSD team with regard to the effects of CNS PPAR-γ on leptin signalling. Leptin signalling in the hypothalamus is blunted in rats fed a HFD, and this leptin resistance is thought to contribute to the continued accumulation of body fat. The Cincinnati team hypothesized that hypothalamic PPAR-γ specifically may contribute to the development of HFD-induced leptin resistance, and that chronic antagonism of CNS PPAR-γ would restore leptin sensitivity these animals. To test this, they administered the PPAR-γ antagonist into the lateral ventricle of HFD-fed rats, at a dose that had no effect on body weight but that did result in significantly lower hypothalamic expression of PPAR-γ’s target gene lipoprotein lipase...
Protein Contributes to Obesity
Weizmann Institute scientists have added another piece to the obesity puzzle, showing how and why a certain protein that is active in a small part of the brain contributes to weight gain. This research appeared in Cell Metabolism.
Prof. Ari Elson and his team in the Institute’s Molecular Genetics Department made the discovery when working with female mice that were genetically engineered to lack this protein, called protein tyrosine phosphatase epsilon (PTPe, for short). The scientists had originally intended to investigate osteoporosis, and thus, they also removed the ovaries of these mice. Taking out ovaries typically causes mice to gain weight to the point of obesity – so the scientists were surprised to find that the weight of the genetically-engineered mice remained stable. Working with Dr. Alon Chen and his group in the Neurobiology Department and Prof. Hilla Knobler, Head of the Unit of Metabolic Disease and Diabetes of Kaplan Medical Center, the researchers fed these mice a high-fat diet, yet the PTPe-deficient mice maintained their svelte figures; they burned more energy and had more stable glucose levels as well...
Prof. Ari Elson and his team in the Institute’s Molecular Genetics Department made the discovery when working with female mice that were genetically engineered to lack this protein, called protein tyrosine phosphatase epsilon (PTPe, for short). The scientists had originally intended to investigate osteoporosis, and thus, they also removed the ovaries of these mice. Taking out ovaries typically causes mice to gain weight to the point of obesity – so the scientists were surprised to find that the weight of the genetically-engineered mice remained stable. Working with Dr. Alon Chen and his group in the Neurobiology Department and Prof. Hilla Knobler, Head of the Unit of Metabolic Disease and Diabetes of Kaplan Medical Center, the researchers fed these mice a high-fat diet, yet the PTPe-deficient mice maintained their svelte figures; they burned more energy and had more stable glucose levels as well...
Monday, May 02, 2011
Eat breakfast to prevent metabolic syndrome
Higher fat at breakfast may be healthier than you think, concludes a new University of Alabama at Birmingham (UAB) study.
According to researchers, the adage "Eat breakfast like a king, lunch like a prince and dinner like a pauper" can be the best advice to follow to prevent metabolic syndrome.
Metabolic syndrome is characterized by abdominal obesity, high triglycerides, insulin resistance and other cardiovascular disease-risk factors.
To reach the conclusion, boffins examined the influence exerted by the type of foods and specific timing of intake on the development of metabolic syndrome characteristics in mice.
The UAB research revealed that mice fed a meal higher in fat after waking had normal metabolic profiles. In contrast, mice that ate a more carbohydrate-rich diet in the morning and consumed a high-fat meal at the end of the day saw increased weight gain, adiposity, glucose intolerance and other markers of the metabolic syndrome...
According to researchers, the adage "Eat breakfast like a king, lunch like a prince and dinner like a pauper" can be the best advice to follow to prevent metabolic syndrome.
Metabolic syndrome is characterized by abdominal obesity, high triglycerides, insulin resistance and other cardiovascular disease-risk factors.
To reach the conclusion, boffins examined the influence exerted by the type of foods and specific timing of intake on the development of metabolic syndrome characteristics in mice.
The UAB research revealed that mice fed a meal higher in fat after waking had normal metabolic profiles. In contrast, mice that ate a more carbohydrate-rich diet in the morning and consumed a high-fat meal at the end of the day saw increased weight gain, adiposity, glucose intolerance and other markers of the metabolic syndrome...
Nutrient in tangerines shown to limit type 2 diabetes risk
The antioxidant nobiletin, which occurs naturally in high levels in tangerines, may help individuals avoid the symptoms of metabolic syndrome and prevent them from developing type 2 diabetes, according to a new study from a group of University of Western Ontario researchers.
Their study, which was published in the journal Diabetes, showed that the molecule prevented mice from experiencing elevated cholesterol levels, high blood pressure, impaired glucose tolerance, buildups of fat in the liver and excess weight gain, even when they were fed a high-fat diet. The mice also showed no signs of type 2 diabetes...
Their study, which was published in the journal Diabetes, showed that the molecule prevented mice from experiencing elevated cholesterol levels, high blood pressure, impaired glucose tolerance, buildups of fat in the liver and excess weight gain, even when they were fed a high-fat diet. The mice also showed no signs of type 2 diabetes...
Saturday, April 30, 2011
Melatonin Might Help Control Weight Gain and Prevent Heart Disease Associated With Obesity
University of Granada researchers have shown that melatonin -- a natural hormone produced by the body -- helps in controlling weight gain, even without reducing the intake of food. Melatonin also improves blood lipid profile, as it reduces triglicerids, and also increases HDL cholesterol and reduces LDL cholesterol.
Melatonin is found in small quantities in some fruits and vegetables as mustard, Goji berries, almonds, sunflower seeds, cardamom, fennel, coriander and cherries. Thus, the intake of this kind of food might help in controlling weight gain and preventing heart diseases associated to obesity and dyslipidemia.
Trials with rats
University of Granada researchers have analyzed in young Zucker diabetic obese rats the effects of melatonin on obesity, dyslipidemia and high blood pressure associated with obesity. Melatonin was found to be beneficial for young rats that had not still developed any metabolic or heart disease. Researchers think that melatonin might help prevent heart disease associated with obesity and dyslipidemia...
Melatonin is found in small quantities in some fruits and vegetables as mustard, Goji berries, almonds, sunflower seeds, cardamom, fennel, coriander and cherries. Thus, the intake of this kind of food might help in controlling weight gain and preventing heart diseases associated to obesity and dyslipidemia.
Trials with rats
University of Granada researchers have analyzed in young Zucker diabetic obese rats the effects of melatonin on obesity, dyslipidemia and high blood pressure associated with obesity. Melatonin was found to be beneficial for young rats that had not still developed any metabolic or heart disease. Researchers think that melatonin might help prevent heart disease associated with obesity and dyslipidemia...
Monday, April 25, 2011
Type 2 diabetes, like Type 1, may be an autoimmune disease, researchers say
Type 2 diabetes, like Type 1, may be an autoimmune disease, but the immune system's target cells are different, Stanford researchers said Sunday. The discovery sheds new light on how obesity contributes to the onset of Type 2 diabetes and could lead to new types of treatment for the disorder, the researchers reported in the journal Nature Medicine.
Diabetes is a growing problem in the United States, triggered in large part by the obesity epidemic. An estimated 27 million Americans are now thought to have diabetes, with the vast majority of them -- all but about a million -- afflicted with Type 2 diabetes. That disorder strikes in adulthood and is marked by a growing inability of cells to respond to insulin in the bloodstream, which necessitates using drugs to increase the output of the hormone by the pancreas. Intriguingly, not everyone who becomes obese develops diabetes, however, and researchers have never been sure why.
Dr. Daniel Winer, an endocrine pathologist now at the University of Toronto, and his twin, Dr. Shawn Winer of the University of Toronto's Hospital for Sick Children, reasoned that the death of excess fat cells might trigger an autoimmune reaction. In an earlier study with senior author Dr. Edgar Engleman of the Stanford University School of Medicine, they demonstrated in mice that, as fat accumulates in the tissues surrounding organs, it outstrips its blood supply, leading to the death of cells on the periphery of the fat deposits. When that occurs, the body mobilizes its immune system to break down and carry off the dead cells. But that produces antibodies against the cells and many of the proteins normally found only inside the cells.
In the new study, the team turned its attention to B cells, the lymphocytes or white blood cells that manufacture antibodies against foreign invaders. They genetically engineered mice so that they could not produce B cells and found that the rodents never became diabetic, no matter how fat they became. They next looked at normal mice that were prone to becoming diabetic when they became obese. One group they treated with a biological drug called anti-CD20 that binds to B cells and blocks their activity. The second group received no treatment. The mice that received the drug did not become diabetic when they became obese, while those that did not receive it did become diabetic. The effect lasted only about 40 days, however, and then needed to be repeated...
Diabetes is a growing problem in the United States, triggered in large part by the obesity epidemic. An estimated 27 million Americans are now thought to have diabetes, with the vast majority of them -- all but about a million -- afflicted with Type 2 diabetes. That disorder strikes in adulthood and is marked by a growing inability of cells to respond to insulin in the bloodstream, which necessitates using drugs to increase the output of the hormone by the pancreas. Intriguingly, not everyone who becomes obese develops diabetes, however, and researchers have never been sure why.
Dr. Daniel Winer, an endocrine pathologist now at the University of Toronto, and his twin, Dr. Shawn Winer of the University of Toronto's Hospital for Sick Children, reasoned that the death of excess fat cells might trigger an autoimmune reaction. In an earlier study with senior author Dr. Edgar Engleman of the Stanford University School of Medicine, they demonstrated in mice that, as fat accumulates in the tissues surrounding organs, it outstrips its blood supply, leading to the death of cells on the periphery of the fat deposits. When that occurs, the body mobilizes its immune system to break down and carry off the dead cells. But that produces antibodies against the cells and many of the proteins normally found only inside the cells.
In the new study, the team turned its attention to B cells, the lymphocytes or white blood cells that manufacture antibodies against foreign invaders. They genetically engineered mice so that they could not produce B cells and found that the rodents never became diabetic, no matter how fat they became. They next looked at normal mice that were prone to becoming diabetic when they became obese. One group they treated with a biological drug called anti-CD20 that binds to B cells and blocks their activity. The second group received no treatment. The mice that received the drug did not become diabetic when they became obese, while those that did not receive it did become diabetic. The effect lasted only about 40 days, however, and then needed to be repeated...
Scientists find treatment for hypertension, obesity
South Korean scientists said Thursday they have found a treatment material that may help people to better deal with hypertension, obesity, and high blood fat.
Researchers led by Lee Chul-ho at the Korea Research Institute of Bioscience and Biotechnology (KRIBB) claimed they isolated a new material called MB12066 that showed promising results in animal tests.
Hypertension currently affects 30 percent of South Korea’s population with the local drug market standing at 1.4 trillion won ($1.3 billion).
“Mice engineered to have high blood pressure and given the MB12066 for six straight weeks showed marked improvements compared to other animals not administered with the new target material,” Lee said...
Researchers led by Lee Chul-ho at the Korea Research Institute of Bioscience and Biotechnology (KRIBB) claimed they isolated a new material called MB12066 that showed promising results in animal tests.
Hypertension currently affects 30 percent of South Korea’s population with the local drug market standing at 1.4 trillion won ($1.3 billion).
“Mice engineered to have high blood pressure and given the MB12066 for six straight weeks showed marked improvements compared to other animals not administered with the new target material,” Lee said...
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