Our team pored over the latest studies, interviewed the top clinicians in obesity science, and listened to the real-life experiences of men and women struggling to maintain their weight. Here, the latest (and often unexpected) thinking behind size and thighs, fatness and fitness...
1. It Really Is Genetic
When scientists first discovered it in certain chubby mice, they called it simply the fatso gene. Years later, when they scoured the human genome for markers that increased vulnerability to type 2 diabetes, the fatso gene (now more politely called FTO) showed up there too. Turns out, people with two copies of the gene were 40 percent more likely to have diabetes and 60 percent more likely to be obese than those without it. Those with only one copy of the gene weighed more too.
Scientists now suspect that there are lots of fat genes.
Saturday, May 29, 2010
$10M Awarded To Einstein For Diabetes Research
The National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) of the National Institutes of Health (NIH) has awarded Albert Einstein College of Medicine of Yeshiva University a five-year, $9.5 million grant for the continuation of its Diabetes Research and Training Center (DRTC). The DRTC was also awarded a $632,000 supplemental grant for equipment and additional pilot and feasibility studies through the American Recovery and Reinvestment Act (ARRA), bringing total NIH support to $10,177,000...
"The ultimate goal of these studies is to develop new therapies for the prevention or treatment of diabetes," said Dr. Pessin. "For example, we recently mapped a signaling pathway that controls energy expenditure in mice. By blocking this pathway, we can increase energy expenditure and cause weight loss in these animals. We're now trying to develop drugs that can interfere with this pathway in humans. If we're successful, we'll take our findings to clinical trials."...
"The ultimate goal of these studies is to develop new therapies for the prevention or treatment of diabetes," said Dr. Pessin. "For example, we recently mapped a signaling pathway that controls energy expenditure in mice. By blocking this pathway, we can increase energy expenditure and cause weight loss in these animals. We're now trying to develop drugs that can interfere with this pathway in humans. If we're successful, we'll take our findings to clinical trials."...
Saturday, May 22, 2010
Sleep apnea ups insulin resistance
The intermittent hypoxia associated with sleep apnea causes a distinct drop in insulin sensitivity in mice, even though chronic hypoxia, such as that associated with high altitude, did not.
The research will be reported at the ATS 2010 International Conference in New Orleans.
To determine whether intermittent hypoxia (IH) and chronic hypoxia (CH) would have different metabolic effects, Dr. Lee and colleagues fitted adult male mice with arterial and venous catheters for continuous rapid blood monitoring of glucose and insulin sensitivity.
They then exposed the mice to either seven hours of IH, in which treatment, oxygen levels oscillated, reaching a low of about 5 percent once a minute, or CH, in which they were exposed to oxygen at a constant rate of 10 percent, and compared each treatment group to protocol-matched controls.
When compared to the control group, the IH mice demonstrated impaired glucose tolerance and reduced insulin sensitivity; the CH group, however, showed only a reduction in glucose tolerance but not insulin sensitivity compared to controls. "Both intermittent hypoxia and continuous hypoxia exposed mice exhibited impaired glucose tolerance, but only the intermittent hypoxia exposed animals demonstrated a reduction in insulin sensitivity," said Euhan John Lee, M.D., a fellow at the Medical Center.
"The intermittent hypoxia of sleep apnea and the continuous hypoxia of altitude are conditions of hypoxic stress that are known to modulate glucose and insulin homeostasis. Although both forms of hypoxia worsen glucose tolerance, this research demonstrated that the increase in insulin resistance that accompanies intermittent hypoxia, or sleep apnea, is greater than that seen with continuous hypoxia, or altitude," explained Dr. Lee.
The specific finding that intermittent, but not continuous, hypoxia induced insulin resistance was not expected.
Increased generation of reactive oxygen species, initiation of pro-inflammatory pathways, elevated sympathetic activity, or upregulation of insulin counter-regulatory hormones in IH may contribute to the greater development of insulin resistance in those mice versus those exposed to continuous hypoxia.
"As sleep apnea continues to rise with the rate of obesity, it will be increasingly important to understand both the independent and interactive effects of both morbidities on the development of metabolic disorders...
The research will be reported at the ATS 2010 International Conference in New Orleans.
To determine whether intermittent hypoxia (IH) and chronic hypoxia (CH) would have different metabolic effects, Dr. Lee and colleagues fitted adult male mice with arterial and venous catheters for continuous rapid blood monitoring of glucose and insulin sensitivity.
They then exposed the mice to either seven hours of IH, in which treatment, oxygen levels oscillated, reaching a low of about 5 percent once a minute, or CH, in which they were exposed to oxygen at a constant rate of 10 percent, and compared each treatment group to protocol-matched controls.
When compared to the control group, the IH mice demonstrated impaired glucose tolerance and reduced insulin sensitivity; the CH group, however, showed only a reduction in glucose tolerance but not insulin sensitivity compared to controls. "Both intermittent hypoxia and continuous hypoxia exposed mice exhibited impaired glucose tolerance, but only the intermittent hypoxia exposed animals demonstrated a reduction in insulin sensitivity," said Euhan John Lee, M.D., a fellow at the Medical Center.
"The intermittent hypoxia of sleep apnea and the continuous hypoxia of altitude are conditions of hypoxic stress that are known to modulate glucose and insulin homeostasis. Although both forms of hypoxia worsen glucose tolerance, this research demonstrated that the increase in insulin resistance that accompanies intermittent hypoxia, or sleep apnea, is greater than that seen with continuous hypoxia, or altitude," explained Dr. Lee.
The specific finding that intermittent, but not continuous, hypoxia induced insulin resistance was not expected.
Increased generation of reactive oxygen species, initiation of pro-inflammatory pathways, elevated sympathetic activity, or upregulation of insulin counter-regulatory hormones in IH may contribute to the greater development of insulin resistance in those mice versus those exposed to continuous hypoxia.
"As sleep apnea continues to rise with the rate of obesity, it will be increasingly important to understand both the independent and interactive effects of both morbidities on the development of metabolic disorders...
Scientists Hope to Trigger Fat-Burning Cells
Last spring, researchers confirmed that brown fat-the kind that burns energy rather than storing it and is especially prevalent in newborns-can be found in small pockets in adults, too, and slimmer adults have more of it. This spring, a team says it might have found one of the first steps in activating that fat-burning fat in adults. Their study comes out in Science this week.
Brown fat is packed with energy-producing mitochondria, and babies have a lot of it because it helps them keep warm. Once humans begin to regulate their own body temperature they don’t need as much brown fat anymore, so it gets replaced by energy-storing white fat, which helps store energy but leads to expanded waistlines in this age of affluence.
Testing on mice, the team led by Stephan Herzig upped the use of an enzyme called cyclooxygenase-2 (COX-2). While the enzyme plays a role in many physiological functions, the researchers found that pushing it in mice could induce their white fat to act more like energy-burning brown fat, and their weight dropped by around 20 percent.
"There has been a lot of excitement around brown fat, but … there wasn’t any clear indication that turning up brown fat would make animals lose weight," says Chad Cowan, a professor in the Department of Stem Cell and Regenerative Biology at Harvard Medical School who studies fat cell development. "What this paper does is make a good link to something that might be clinically beneficial."
Don’t get too excited just yet. This is a test on mice, not people, and there’s another problem: This transformation in the animals, white fat acting like brown fat, happened only when Herzig and his colleagues tricked the mice’s bodies into thinking they were at a colder temperature than they actually were: That caveat is important because the COX-2 enzyme is present in a wide range of body tissues, and revving up its activity may lead to some serious side effects such as clotting problems, increased sensitivity to pain and even muscle abnormalities. Herzig found that manipulating the COX-2 pathway switched white fat to brown fat in the mice only when he simulated cold temperatures through metabolic tweaks - dilating small blood vessels and increasing the pumping of the heart - and made the rodents act as if they were shivering...
Brown fat is packed with energy-producing mitochondria, and babies have a lot of it because it helps them keep warm. Once humans begin to regulate their own body temperature they don’t need as much brown fat anymore, so it gets replaced by energy-storing white fat, which helps store energy but leads to expanded waistlines in this age of affluence.
Testing on mice, the team led by Stephan Herzig upped the use of an enzyme called cyclooxygenase-2 (COX-2). While the enzyme plays a role in many physiological functions, the researchers found that pushing it in mice could induce their white fat to act more like energy-burning brown fat, and their weight dropped by around 20 percent.
"There has been a lot of excitement around brown fat, but … there wasn’t any clear indication that turning up brown fat would make animals lose weight," says Chad Cowan, a professor in the Department of Stem Cell and Regenerative Biology at Harvard Medical School who studies fat cell development. "What this paper does is make a good link to something that might be clinically beneficial."
Don’t get too excited just yet. This is a test on mice, not people, and there’s another problem: This transformation in the animals, white fat acting like brown fat, happened only when Herzig and his colleagues tricked the mice’s bodies into thinking they were at a colder temperature than they actually were: That caveat is important because the COX-2 enzyme is present in a wide range of body tissues, and revving up its activity may lead to some serious side effects such as clotting problems, increased sensitivity to pain and even muscle abnormalities. Herzig found that manipulating the COX-2 pathway switched white fat to brown fat in the mice only when he simulated cold temperatures through metabolic tweaks - dilating small blood vessels and increasing the pumping of the heart - and made the rodents act as if they were shivering...
Researcher Calls Out Laboratory ‘Flab Rats’
A medical researcher is calling out laboratory “flab rats” for their obesity and lack of exercise — and he’s not talking about unfit grad students existing on vending-machine candy . He really means the rats (and mice) themselves, the condition of which he says may be leading “to spurious experimental results.”
Writing in New Scientist, Mark Mattson, chief of the laboratory of neurosciences at the U.S. National Institute on Aging Intramural Research Program, argues that rodents used in experiments are overfed and under-exercised, resulting in health problems that may make them poor research subjects. High blood sugar, high blood pressure, cholesterol problems and obesity, among other ailments, all make them more susceptible to certain diseases and may skew results.
How bad is it? “Some strains of lab rat attain a body weight in excess of 1 kilogram, nearly double that of a healthy rat,” he writes. (We think we’ve actually seen one of those on the NYC subway tracks.)
Here’s what Mattson has to say about implications for cancer research:
We know that some carcinogens are more potent in overweight animals and that couch-potato rodents have an elevated risk of developing tumors. In addition, many types of tumor grow more rapidly in animals with unlimited access to food, and certain aspects of metastasis — the process by which tumors spread to new sites in the body — appear to differ between obese and slender mice. Experimental cancer drugs might therefore act differently in couch-potato individuals than in their slender counterparts.
The researcher writes that animal models for neurodegenerative diseases, cardiovascular diseases and renal problems may also be inaccurate if the animals are fat and out of shape. To better mimic the effects of potential treatments in humans who exercise and are at a healthy weight, he suggests withholding food and providing exercise wheels to some of the rodents being used in experiments...
Writing in New Scientist, Mark Mattson, chief of the laboratory of neurosciences at the U.S. National Institute on Aging Intramural Research Program, argues that rodents used in experiments are overfed and under-exercised, resulting in health problems that may make them poor research subjects. High blood sugar, high blood pressure, cholesterol problems and obesity, among other ailments, all make them more susceptible to certain diseases and may skew results.
How bad is it? “Some strains of lab rat attain a body weight in excess of 1 kilogram, nearly double that of a healthy rat,” he writes. (We think we’ve actually seen one of those on the NYC subway tracks.)
Here’s what Mattson has to say about implications for cancer research:
We know that some carcinogens are more potent in overweight animals and that couch-potato rodents have an elevated risk of developing tumors. In addition, many types of tumor grow more rapidly in animals with unlimited access to food, and certain aspects of metastasis — the process by which tumors spread to new sites in the body — appear to differ between obese and slender mice. Experimental cancer drugs might therefore act differently in couch-potato individuals than in their slender counterparts.
The researcher writes that animal models for neurodegenerative diseases, cardiovascular diseases and renal problems may also be inaccurate if the animals are fat and out of shape. To better mimic the effects of potential treatments in humans who exercise and are at a healthy weight, he suggests withholding food and providing exercise wheels to some of the rodents being used in experiments...
Male, female fat cells different in mice
Genes dictate if fat is stored on belly or hips -- in particular, gender genes, U.S. researchers said.
Researchers at the University of Texas Southwestern Medical Center in Dallas, who studied mice say they were surprised to find major differences between male and female fat cells.
"We found that out of about 40,000 mouse genes, only 138 are commonly found in both male and female fat cells," senior author Dr. Deborah Clegg said in a statement. "This was completely unexpected. We expected the exact opposite -- that 138 would be different and the rest would be the same between the sexes."
The study, published in the International Journal of Obesity, also found male mice on a high-fat diet gained more weight and had more highly inflamed fat tissue -- especially belly fat -- than female mice eating the same diet.
However, in the female mice whose ovaries had been removed -- a condition similar to human menopause -- put on the high fat diet, weight gain was greater and more likely to be in the belly...
Researchers at the University of Texas Southwestern Medical Center in Dallas, who studied mice say they were surprised to find major differences between male and female fat cells.
"We found that out of about 40,000 mouse genes, only 138 are commonly found in both male and female fat cells," senior author Dr. Deborah Clegg said in a statement. "This was completely unexpected. We expected the exact opposite -- that 138 would be different and the rest would be the same between the sexes."
The study, published in the International Journal of Obesity, also found male mice on a high-fat diet gained more weight and had more highly inflamed fat tissue -- especially belly fat -- than female mice eating the same diet.
However, in the female mice whose ovaries had been removed -- a condition similar to human menopause -- put on the high fat diet, weight gain was greater and more likely to be in the belly...
Anti-obesity effect of an isoflavone fatty acid ester on obese mice induced by high fat diet and its potential mechanism
The novel compound 1a is one of the isoflavone fatty acid esters. In order to investigate the anti-obesity effect of compound 1a and its potential mechanism of influence in adipocyte differentiation, Obese male C57BL/6J mice induced by high-fat diet (HFD) and rat preadipocytes3T3-L1 cellwere used.MethodAfter 4-week HFD induction, the obese model was made successfully...
Conclusion: Compound 1a regulates serum lipid profiles, decreases adipose tissue mass and body weight gain by inducing adipocyte apoptosis in high fat diet induced mice.
Thus, it may be used to treat obese patients with hypercholesterolemia and hypertriglyceridemia.
Conclusion: Compound 1a regulates serum lipid profiles, decreases adipose tissue mass and body weight gain by inducing adipocyte apoptosis in high fat diet induced mice.
Thus, it may be used to treat obese patients with hypercholesterolemia and hypertriglyceridemia.
Sunday, May 16, 2010
Belly Fat or Hip Fat: It Really Is All in Your Genes, Says Researcher
The age-old question of why men store fat in their bellies and women store it in their hips may have finally been answered: Genetically speaking, the fat tissue is almost completely different.
"We found that out of about 40,000 mouse genes, only 138 are commonly found in both male and female fat cells," said Dr. Deborah Clegg, assistant professor of internal medicine at UT Southwestern Medical Center and senior author of the study appearing in the International Journal of Obesity. "This was completely unexpected. We expected the exact opposite -- that 138 would be different and the rest would be the same between the sexes."
The study involved mice, which distribute their fat in a sexually dimorphic pattern similar to humans.
"Given the difference in gene expression profiles, a female fat tissue won't behave anything like a male fat tissue and vice versa," Dr. Clegg said. "The notion that fat cells between males and females are alike is inconsistent with our findings."
In humans, men are more likely to carry extra weight around their guts while pre-menopausal women store it in their butts, thighs and hips. The bad news for men is that belly, or visceral, fat has been associated with numerous obesity-related diseases including diabetes and heart disease. Women, on the other hand, are generally protected from these obesity-related disorders until menopause, when their ovarian hormone levels drop and fat storage tends to shift from their rear ends to their waists.
"Although our new findings don't explain why women begin storing fat in their bellies after menopause, the results do bring us a step closer to understanding the mechanisms behind the unwanted shift," Dr. Clegg said.
For this study, researchers used a microarray analysis to determine whether male fat cells and female fat cells were different between the waist and hips and if they were different based on gender at a genetic level.
Because the fat distribution patterns of male and female mice are similar to those of humans, the researchers used the animals to compare genes from the belly and hip fat pads of male mice, female mice and female mice whose ovaries had been removed -- a condition that closely mimics human menopause. Waist and hip fat (subcutaneous fat) generally accumulates outside the muscle wall, whereas belly fat (visceral fat), a major health concern in men and postmenopausal women, develops around the internal organs.
In addition to the genetic differences among fat tissues, the researchers found that male mice that consumed a high-fat diet for 12 weeks gained more weight than female mice on the same diet. The males' fat tissue, particularly their belly fat, became highly inflamed, while the females had lower levels of genes associated with inflammation. The female mice whose ovaries had been removed, however, gained weight on the high-fat diet more like the males and deposited this fat in their bellies, also like the males.
"The fat of the female mice whose ovaries had been removed was inflamed and was starting to look like the unhealthy male fat," Dr. Clegg said. "However, estrogen replacement therapy in the mice reduced the inflammation and returned their fat distribution to that of mice with their ovaries intact."
Dr. Clegg said the results suggest that hormones made by the ovaries may be critical in determining where fat is deposited. Her overall goal is to determine how fat tissue is affected by sex hormones and whether it would be possible to develop a "designer" hormone replacement therapy that protected postmenopausal women from belly fat and related diseases such as metabolic syndrome...
"We found that out of about 40,000 mouse genes, only 138 are commonly found in both male and female fat cells," said Dr. Deborah Clegg, assistant professor of internal medicine at UT Southwestern Medical Center and senior author of the study appearing in the International Journal of Obesity. "This was completely unexpected. We expected the exact opposite -- that 138 would be different and the rest would be the same between the sexes."
The study involved mice, which distribute their fat in a sexually dimorphic pattern similar to humans.
"Given the difference in gene expression profiles, a female fat tissue won't behave anything like a male fat tissue and vice versa," Dr. Clegg said. "The notion that fat cells between males and females are alike is inconsistent with our findings."
In humans, men are more likely to carry extra weight around their guts while pre-menopausal women store it in their butts, thighs and hips. The bad news for men is that belly, or visceral, fat has been associated with numerous obesity-related diseases including diabetes and heart disease. Women, on the other hand, are generally protected from these obesity-related disorders until menopause, when their ovarian hormone levels drop and fat storage tends to shift from their rear ends to their waists.
"Although our new findings don't explain why women begin storing fat in their bellies after menopause, the results do bring us a step closer to understanding the mechanisms behind the unwanted shift," Dr. Clegg said.
For this study, researchers used a microarray analysis to determine whether male fat cells and female fat cells were different between the waist and hips and if they were different based on gender at a genetic level.
Because the fat distribution patterns of male and female mice are similar to those of humans, the researchers used the animals to compare genes from the belly and hip fat pads of male mice, female mice and female mice whose ovaries had been removed -- a condition that closely mimics human menopause. Waist and hip fat (subcutaneous fat) generally accumulates outside the muscle wall, whereas belly fat (visceral fat), a major health concern in men and postmenopausal women, develops around the internal organs.
In addition to the genetic differences among fat tissues, the researchers found that male mice that consumed a high-fat diet for 12 weeks gained more weight than female mice on the same diet. The males' fat tissue, particularly their belly fat, became highly inflamed, while the females had lower levels of genes associated with inflammation. The female mice whose ovaries had been removed, however, gained weight on the high-fat diet more like the males and deposited this fat in their bellies, also like the males.
"The fat of the female mice whose ovaries had been removed was inflamed and was starting to look like the unhealthy male fat," Dr. Clegg said. "However, estrogen replacement therapy in the mice reduced the inflammation and returned their fat distribution to that of mice with their ovaries intact."
Dr. Clegg said the results suggest that hormones made by the ovaries may be critical in determining where fat is deposited. Her overall goal is to determine how fat tissue is affected by sex hormones and whether it would be possible to develop a "designer" hormone replacement therapy that protected postmenopausal women from belly fat and related diseases such as metabolic syndrome...
Saturday, May 15, 2010
New way found to boost good cholesterol in mice
Two research teams have found a new way to increase levels of so-called "good" cholesterol in mice, they said on Thursday in a finding that could lead to better ways to prevent heart disease in humans...
Sunday, May 09, 2010
Slimming Aid from the Cell Laboratory? Inflammation Enzyme Regulates the Production of Brown Fat Tissue
Scientists of the German Cancer Research Center (Deutsches Krebsforschungszentrum, DKFZ) have published an article in Science revealing that the COX-2 inflammation enzyme stimulates the formation of new brown fat tissue in mice. Brown fat tissue transforms energy into heat. Therefore, mice with increased COX-2 production have a higher energy consumption and are slimmer. On the basis of these results scientists might develop a novel weight loss method for pathogenic obesity.
Love handles, muffin tops and stomach tires -- white fat tissue forms the typical curves in the notorious problem areas to store energy. Exactly the opposite happens in brown fat tissue: Instead of being stored, energy gets transformed into heat. To the dismay of many people, adults have only small amounts of this energy burner. By contrast, babies and animals in hibernation have lots of it in their bodies where it serves for heat regulation.
Researchers know that external influences can stimulate the production of brown fat tissue in animals. If rodents are kept at low temperatures, clusters of brown fat cells form amid the white fat tissue. A DKFZ research team headed by Dr. Stephan Herzig, jointly with colleagues from Munich, Marburg, Frankfurt and Lausanne, has investigated the molecular causes of this phenomenon. They discovered that the production of the COX-2 inflammation enzyme is increased in white fat tissue of mice after exposure to cold temperatures. COX-2 is well known to scientists: It regulates the key step in the biosynthesis of prostaglandins -- inflammation-promoting hormones which are also responsible for activating pain...
Even without using cold temperatures the scientists were able to stimulate the formation of brown fat cell clusters in white fat tissue by boosting the COX-2 production in mice using a molecular-biological trick. The body weight of these animals was 20 percent lower than that of normal animals. Even on a calorie-rich diet they did not put on weight.
Love handles, muffin tops and stomach tires -- white fat tissue forms the typical curves in the notorious problem areas to store energy. Exactly the opposite happens in brown fat tissue: Instead of being stored, energy gets transformed into heat. To the dismay of many people, adults have only small amounts of this energy burner. By contrast, babies and animals in hibernation have lots of it in their bodies where it serves for heat regulation.
Researchers know that external influences can stimulate the production of brown fat tissue in animals. If rodents are kept at low temperatures, clusters of brown fat cells form amid the white fat tissue. A DKFZ research team headed by Dr. Stephan Herzig, jointly with colleagues from Munich, Marburg, Frankfurt and Lausanne, has investigated the molecular causes of this phenomenon. They discovered that the production of the COX-2 inflammation enzyme is increased in white fat tissue of mice after exposure to cold temperatures. COX-2 is well known to scientists: It regulates the key step in the biosynthesis of prostaglandins -- inflammation-promoting hormones which are also responsible for activating pain...
Even without using cold temperatures the scientists were able to stimulate the formation of brown fat cell clusters in white fat tissue by boosting the COX-2 production in mice using a molecular-biological trick. The body weight of these animals was 20 percent lower than that of normal animals. Even on a calorie-rich diet they did not put on weight.
Saturday, May 08, 2010
A potential new treatment for Type 2 diabetes
Australian scientists propose that a drug, already being used to treat rare inherited disorders, may also help people with Type 2 diabetes.
Type 2 diabetes occurs when the body no longer controls blood sugar levels properly. We need insulin, a hormone made in the pancreas, to channel sugar from our blood into our cells. The insulin-producing cells of the pancreas, known as ‘islets’ or ‘beta cells’, become progressively less efficient in people with Type 2 diabetes. At the same time, their muscles become less responsive to insulin, a condition known as ‘insulin resistance’. The combined result is high blood sugar levels, which can be very damaging to blood vessels and organs.
Kim Cheng and Drs Kenneth Ho and Jenny Gunton from Sydney’s Garvan Institute of Medical Research, show that the reduced expression of the HIF-1 alpha gene in beta cells – with the resulting reduction of HIF-1 alpha protein – helps explain the impaired ability of the pancreas to produce insulin in people with Type 2 diabetes. More importantly though, they were able to show that administering a drug (already approved for another rare disorder) increased levels of HIF-1 alpha protein and may restore insulin production. The findings are now online in the Journal of Clinical Investigation.
“We believe that HIF-1 alpha is a key player, effectively orchestrating many events in the cell that eventually start to shut down insulin secretion,” said Dr Gunton.
“HIF-1 alpha is a transcription factor, which means that it controls the way genes are expressed, or transcribed. This particular transcription factor happens to impact many genes that affect glucose uptake and metabolism in the pancreas. So when it is low, the beta cells have less energy.”
“Beta cells secrete insulin when they detect an increase in their own energy. When they can’t ‘see’ glucose, as rising energy, they don’t secrete insulin.”
The group tested and confirmed the importance of HIF-1 alpha in several ways.
First, they genetically engineered mice without the HIF-1 alpha gene in beta cells. These mice were mildly glucose intolerant, meaning that their blood sugar levels were higher than normal.
Next, they replicated the animal findings in cultured islets, in which the levels of HIF-1 alpha protein had been reduced.
After that, they fed genetically engineered and normal mice a high fat diet to make them fat and induce insulin resistance. Under these conditions, glucose levels deteriorate rapidly because beta cells are forced to work much harder to maintain normal sugar levels.
When all the mice were given the drug to stimulate the production of HIF-1 alpha protein, glucose levels improved in the ‘normal’ mice, despite the fact they continued on a high fat diet. The drug had absolutely no effect on the mice without the HIF-1 alpha gene in their beta cells.
“These tests left no doubt that it’s beta cell HIF-1 alpha that is needed for this drug to affect glucose tolerance,” said Gunton.
“Once we’d established that, we did a new study treating the ‘normal’ mice for six months to establish the drug’s safety over the longer-term. We did not detect side effects and the mice developed better glucose tolerance.”
“Then to be really thorough, we showed the same results in a completely different genetic line of mice.”
Type 2 diabetes occurs when the body no longer controls blood sugar levels properly. We need insulin, a hormone made in the pancreas, to channel sugar from our blood into our cells. The insulin-producing cells of the pancreas, known as ‘islets’ or ‘beta cells’, become progressively less efficient in people with Type 2 diabetes. At the same time, their muscles become less responsive to insulin, a condition known as ‘insulin resistance’. The combined result is high blood sugar levels, which can be very damaging to blood vessels and organs.
Kim Cheng and Drs Kenneth Ho and Jenny Gunton from Sydney’s Garvan Institute of Medical Research, show that the reduced expression of the HIF-1 alpha gene in beta cells – with the resulting reduction of HIF-1 alpha protein – helps explain the impaired ability of the pancreas to produce insulin in people with Type 2 diabetes. More importantly though, they were able to show that administering a drug (already approved for another rare disorder) increased levels of HIF-1 alpha protein and may restore insulin production. The findings are now online in the Journal of Clinical Investigation.
“We believe that HIF-1 alpha is a key player, effectively orchestrating many events in the cell that eventually start to shut down insulin secretion,” said Dr Gunton.
“HIF-1 alpha is a transcription factor, which means that it controls the way genes are expressed, or transcribed. This particular transcription factor happens to impact many genes that affect glucose uptake and metabolism in the pancreas. So when it is low, the beta cells have less energy.”
“Beta cells secrete insulin when they detect an increase in their own energy. When they can’t ‘see’ glucose, as rising energy, they don’t secrete insulin.”
The group tested and confirmed the importance of HIF-1 alpha in several ways.
First, they genetically engineered mice without the HIF-1 alpha gene in beta cells. These mice were mildly glucose intolerant, meaning that their blood sugar levels were higher than normal.
Next, they replicated the animal findings in cultured islets, in which the levels of HIF-1 alpha protein had been reduced.
After that, they fed genetically engineered and normal mice a high fat diet to make them fat and induce insulin resistance. Under these conditions, glucose levels deteriorate rapidly because beta cells are forced to work much harder to maintain normal sugar levels.
When all the mice were given the drug to stimulate the production of HIF-1 alpha protein, glucose levels improved in the ‘normal’ mice, despite the fact they continued on a high fat diet. The drug had absolutely no effect on the mice without the HIF-1 alpha gene in their beta cells.
“These tests left no doubt that it’s beta cell HIF-1 alpha that is needed for this drug to affect glucose tolerance,” said Gunton.
“Once we’d established that, we did a new study treating the ‘normal’ mice for six months to establish the drug’s safety over the longer-term. We did not detect side effects and the mice developed better glucose tolerance.”
“Then to be really thorough, we showed the same results in a completely different genetic line of mice.”
Australian researchers optimistic of new diabetes treatment
Australian researchers are hopeful they've found a new way to treat type 2 diabetes.
The World Health Organisation says in the Pacific, chronic diseases such as diabetes and cardiovascular diseases are among the most serious health problems.
The disease is associated with poor diet, lack of exercise and obesity.
In the study using mice, the researchers from Sydney's Garvin Institute of Medical Research found a way to switch on the insulin producing cells in the pancreas that all but stop working in people with diabetes...
The World Health Organisation says in the Pacific, chronic diseases such as diabetes and cardiovascular diseases are among the most serious health problems.
The disease is associated with poor diet, lack of exercise and obesity.
In the study using mice, the researchers from Sydney's Garvin Institute of Medical Research found a way to switch on the insulin producing cells in the pancreas that all but stop working in people with diabetes...
Scientists find anxiety gene that also makes you comfort eat
Researchers have found an "anxiety gene" which when switched on not only causes stress but increases our craving for sweets and comfort food.
They believe that the gene could be the reason why we are becoming an increasingly obese and stressful society. It could be the reason for the phenomenon "comfort eating".
Dr Alon Chen, a neuroendocrinologist at the Weizmann Institute in Israel, said: "We showed that the actions of a single gene in just one part of the brain can have profound effects on the metabolism of the whole body.
"In essence, stress may be turning us fat."
Few people lead stress-free lives these days which may, say experts, account for the rise in obesity triggered by the stress gene.
"Stress is definitely influencing every system in the body," said Dr Chen "It's not just causing anxiety, depression and post-traumatic stress disorder but is influencing metabolic syndromes such as obesity."
In the study, published in the Proceedings of the National Academy of Sciences, the researchers have discovered that there's a "stress switch" that seems to lead to diabetes and obesity.
The Israeli researchers created their own method for changing the activity of the gene in the brain, causing it to release varied amounts of a protein called Ucn3.
They discovered that increased levels of Ucn3 caused anxiety and changes in metabolism.
With increased levels of Ucn3, the bodies of mice used more sugar and less fatty acids and metabolic rates increased, showing the first stages of type 2 diabetes...
They believe that the gene could be the reason why we are becoming an increasingly obese and stressful society. It could be the reason for the phenomenon "comfort eating".
Dr Alon Chen, a neuroendocrinologist at the Weizmann Institute in Israel, said: "We showed that the actions of a single gene in just one part of the brain can have profound effects on the metabolism of the whole body.
"In essence, stress may be turning us fat."
Few people lead stress-free lives these days which may, say experts, account for the rise in obesity triggered by the stress gene.
"Stress is definitely influencing every system in the body," said Dr Chen "It's not just causing anxiety, depression and post-traumatic stress disorder but is influencing metabolic syndromes such as obesity."
In the study, published in the Proceedings of the National Academy of Sciences, the researchers have discovered that there's a "stress switch" that seems to lead to diabetes and obesity.
The Israeli researchers created their own method for changing the activity of the gene in the brain, causing it to release varied amounts of a protein called Ucn3.
They discovered that increased levels of Ucn3 caused anxiety and changes in metabolism.
With increased levels of Ucn3, the bodies of mice used more sugar and less fatty acids and metabolic rates increased, showing the first stages of type 2 diabetes...
Differences in disease risk for men and women start in the womb
Washington, DC: Disease risk in later life differs for women and men and now scientists have shown that this may start in the womb.
Pregnancy places competing demands on a mother's physiology: Her body wants to produce a strong healthy baby but not at the expense of her own health. Some of the genes that she passes on to her child therefore try to protect her own body from excessive demands from her child.
These so-called "imprinted genes" inherited from the father however do not show the same restraint - their goal is to get as many resources for the foetus as possible.
"The imprinted genes derived from the father are greedy whilst those from the mother are conservative in their needs to ensure future reproductive success", said Dr. Miguel Constancia from the University of Cambridge, England.
"We have found evidence that imprinted genes play important roles in the control of endocrine functions of the placenta. These placental adaptations have marked effects on nutrient delivery to the foetus, resulting in the programming of homeostatic mechanisms with metabolic consequences extending to adulthood, for example for type 2 diabetes susceptibility," Constancia added.
There is evidence that some programming effects are different in male and female offspring.
Dr. Rachel Dakin from the University of Edinburgh, Scotland, shows how maternal obesity is associated with sex-specific programming effects in young adult mice. Female offspring of obese mothers had raised blood insulin levels, whilst male offspring did not. Male offspring did have alterations in the expression of liver genes important in lipid and glucocorticoid metabolism...
Pregnancy places competing demands on a mother's physiology: Her body wants to produce a strong healthy baby but not at the expense of her own health. Some of the genes that she passes on to her child therefore try to protect her own body from excessive demands from her child.
These so-called "imprinted genes" inherited from the father however do not show the same restraint - their goal is to get as many resources for the foetus as possible.
"The imprinted genes derived from the father are greedy whilst those from the mother are conservative in their needs to ensure future reproductive success", said Dr. Miguel Constancia from the University of Cambridge, England.
"We have found evidence that imprinted genes play important roles in the control of endocrine functions of the placenta. These placental adaptations have marked effects on nutrient delivery to the foetus, resulting in the programming of homeostatic mechanisms with metabolic consequences extending to adulthood, for example for type 2 diabetes susceptibility," Constancia added.
There is evidence that some programming effects are different in male and female offspring.
Dr. Rachel Dakin from the University of Edinburgh, Scotland, shows how maternal obesity is associated with sex-specific programming effects in young adult mice. Female offspring of obese mothers had raised blood insulin levels, whilst male offspring did not. Male offspring did have alterations in the expression of liver genes important in lipid and glucocorticoid metabolism...
Study finds what makes calorie-burning "brown fat"
The discovery may help researchers develop ways to fight the obesity epidemic that is sucking up health budgets and resources in rich nations and quickly spreading to the developing world.
Stephan Herzig of the German Cancer Research Center in Heidelberg, who led the study, said scientists could now try using stem cells to generate brown fat cells in a lab dish to then implant them into the body and help speed up calorie burn.
"Now that we know some of the signals that are required to generate brown cells, we have the tools to put everything together and try it out," he said in a telephone interview.
Stem cells are the driver cells from which all other cells develop.
Rates of obesity have risen dramatically in recent decades in affluent nations, and more Western-style diets and less exercise mean that corpulence is taking hold in developing populations too.
Already, two-thirds of U.S. adults and nearly one in three children are overweight or obese -- a condition that increases risks of diabetes, heart disease and other chronic illnesses.
FOX-2 ENZYME IS THE TRIGGER
Experimenting on mice in the lab, Herzig and a team of scientists in Germany and Switzerland found that an enzyme called COX-2 triggers development of fat cells to become brown fat, instead of white fat.
White adipose tissue hoards fat by using our bodies -- particularly our bellies and thighs -- as a large storage unit, while brown adipose tissue is a sparse form of fat that helps keep newborns warm and helps adults burn calories.
Once activated by cold temperatures, brown fat burns calories faster than regular fat.
The researchers, whose study was published in the journal Science on Thursday, also found that mice who were genetically engineered to produce high levels of COX-2 burned energy faster and were protected from obesity.
Scientists estimate that as little as 50 grams of brown adipose tissue in a normal adult human would be enough to increase energy consumption by 20 percent...
Stephan Herzig of the German Cancer Research Center in Heidelberg, who led the study, said scientists could now try using stem cells to generate brown fat cells in a lab dish to then implant them into the body and help speed up calorie burn.
"Now that we know some of the signals that are required to generate brown cells, we have the tools to put everything together and try it out," he said in a telephone interview.
Stem cells are the driver cells from which all other cells develop.
Rates of obesity have risen dramatically in recent decades in affluent nations, and more Western-style diets and less exercise mean that corpulence is taking hold in developing populations too.
Already, two-thirds of U.S. adults and nearly one in three children are overweight or obese -- a condition that increases risks of diabetes, heart disease and other chronic illnesses.
FOX-2 ENZYME IS THE TRIGGER
Experimenting on mice in the lab, Herzig and a team of scientists in Germany and Switzerland found that an enzyme called COX-2 triggers development of fat cells to become brown fat, instead of white fat.
White adipose tissue hoards fat by using our bodies -- particularly our bellies and thighs -- as a large storage unit, while brown adipose tissue is a sparse form of fat that helps keep newborns warm and helps adults burn calories.
Once activated by cold temperatures, brown fat burns calories faster than regular fat.
The researchers, whose study was published in the journal Science on Thursday, also found that mice who were genetically engineered to produce high levels of COX-2 burned energy faster and were protected from obesity.
Scientists estimate that as little as 50 grams of brown adipose tissue in a normal adult human would be enough to increase energy consumption by 20 percent...
Friday, April 30, 2010
Gene that ties stress to diabetes, depression identified
Researchers have identified the gene changes in whose activity due to stress cause anxiety disorders and depression, as well as metabolic disorders like obesity, type 2 diabetes and arteriosclerosis.
These diseases, linked to stress, are reaching epidemic proportions.
Alon Chen of the Weizmann Institute's Neurobiology Department and his research team have now discovered that changes in the activity of a single gene in the brain not only cause mice to exhibit anxious behaviour but also lead to metabolic changes that cause the mice to develop symptoms associated with type 2 diabetes...
These diseases, linked to stress, are reaching epidemic proportions.
Alon Chen of the Weizmann Institute's Neurobiology Department and his research team have now discovered that changes in the activity of a single gene in the brain not only cause mice to exhibit anxious behaviour but also lead to metabolic changes that cause the mice to develop symptoms associated with type 2 diabetes...
Obesity epidemic blamed on bacteria
Previous research has shown that intestinal bacteria populations differ between the obese and the lean in humans. A new study using mice shows that increased appetite and insulin resistance can be transferred by intestinal bacteria from one mouse to another. This indicates that the presence of the intestinal bacterial contributes to changes in both appetite and metabolism.
The team at Emory were studying mice with an altered immune system so that they lacked Toll-like receptor 5 (TLR5), a receptor that recognises flagellin, and therefore the presence of bacteria. The TLR5 deficient mice were heavier than their normal counterparts and also consumed more food. They had metabolic changes associated with obesity. When the TLR5 deficient mice were fed a restricted diet, they remained insulin resistant. When given a full-fat diet, they developed diabetes and fatty liver disease. When TLR5 deficient mice were given strong antibiotics, enough to kill most of their intestinal flora, their metabolic abnormalities decreased. Studying the gut flora of TLR5 deficient mice and normal mice showed differing compositions of bacterial families. Previous research has already shown that the components of gut flora can alter the ability of the intestines to extract calories from food...
The team at Emory were studying mice with an altered immune system so that they lacked Toll-like receptor 5 (TLR5), a receptor that recognises flagellin, and therefore the presence of bacteria. The TLR5 deficient mice were heavier than their normal counterparts and also consumed more food. They had metabolic changes associated with obesity. When the TLR5 deficient mice were fed a restricted diet, they remained insulin resistant. When given a full-fat diet, they developed diabetes and fatty liver disease. When TLR5 deficient mice were given strong antibiotics, enough to kill most of their intestinal flora, their metabolic abnormalities decreased. Studying the gut flora of TLR5 deficient mice and normal mice showed differing compositions of bacterial families. Previous research has already shown that the components of gut flora can alter the ability of the intestines to extract calories from food...
Monday, April 26, 2010
Chokeberry Extract Found to Regulate Weight Gain, Blood Glucose, and Inflammation in Rats
Chokeberry bushes have for centuries been residents of eastern deciduous forests where their bright red and dark purple fruits continue to be favorite snacks of local bird species. Native Americans have also traditionally eaten dried chokeberries and prepared teas from parts of the plant, and several domesticated varieties now grace contemporary lawns and gardens from coast to coast. However, the chokeberry (Aronia) is enjoying a new claim-to-fame as a potentially powerful antioxidant, and can now be found for sale in the dietary supplement and "health food" aisles of your local pharmacies and grocery stores.
What makes the humble chokeberry so healthful? Scientists think the answer lies in their unusually high levels of substances called anthocyanins (from the Greek anthos + kyanos meaning dark blue). There are many different anthocyanins in these colorful berries, but they all function as antioxidants -- originally protecting the chokeberry seed from sunshine-induced oxidative stress. And when we eat them, they also appear to protect our bodies from a variety of damaging situations, including exposure to pollution and metabolically-derived free radicals. Indeed, a growing body of scientific literature has shown promising effects of chokeberry consumption on diseases ranging from cancer to obesity. These health-promoting effects may be due to the potent anti-inflammatory properties of anthocyanins, as uncontrolled inflammation is now universally recognized as a common thread in many of our most prevalent and deadly diseases. In addition, certain anthocyanins -- including those found in chokeberry -- have also been shown to improve blood sugar and the function of insulin.
To better understand how chokeberries influence health, Drs. Bolin Qin and Richard Anderson from the US Department of Agriculture in Beltsville, MD studied what happens when prediabetic rats are fed chokeberry extracts for an extended period of time. The results of their research were presented on April 25 at the Experimental Biology 2010 meeting in Anaheim, CA. This presentation is part of the scientific program of the American Society for Nutrition, home of the world's leading nutrition researchers.
The researchers first made 18 male rats "prediabetic" or insulin insensitive by feeding them a fructose-rich diet for 6 weeks. Then they randomized the animals to continue drinking either pure water or water spiked with low or high levels of chokeberry extract (CellBerry®, Integrity Nutraceuticals International). After drinking this water for 6 weeks, the groups were compared in terms of body weight, body fat, blood glucose regulation, and molecular markers for inflammation.
Qin and Anderson found that at the end of the study the rats consuming the chokeberry-spiked water weighed less than the controls; both levels of chokeberry had the same effect in this regard. Similar beneficial effects of chokeberry consumption were found for body fat (specifically, that of the lower abdominal region). They also discovered that animals that had been drinking chokeberry extract had lower blood glucose and reduced levels of plasma triglycerides, cholesterol, and low-density lipoprotein (LDL) cholesterol when compared to the control animals. These alterations would theoretically lead to lower risk for diabetes and cardiovascular disease in humans. And to add even more evidence for a healthful impact of this super-berry, the researchers documented numerous alterations in expression of genes that would likely lead to reduced chronic inflammation and perhaps even lower cancer risk. For instance, drinking chokeberry extract lowered expression of the gene coding for interleukin-6 (IL-6), a protein that normally triggers inflammation following trauma or infection. Chronic overproduction of IL-6 has been documented in many diseases such as diabetes, arthritis, and atherosclerosis and is thought to be a partial cause of these conditions.
Of course, human studies will be needed before scientists can declare whether we derive the same health benefits from the chokeberry...
What makes the humble chokeberry so healthful? Scientists think the answer lies in their unusually high levels of substances called anthocyanins (from the Greek anthos + kyanos meaning dark blue). There are many different anthocyanins in these colorful berries, but they all function as antioxidants -- originally protecting the chokeberry seed from sunshine-induced oxidative stress. And when we eat them, they also appear to protect our bodies from a variety of damaging situations, including exposure to pollution and metabolically-derived free radicals. Indeed, a growing body of scientific literature has shown promising effects of chokeberry consumption on diseases ranging from cancer to obesity. These health-promoting effects may be due to the potent anti-inflammatory properties of anthocyanins, as uncontrolled inflammation is now universally recognized as a common thread in many of our most prevalent and deadly diseases. In addition, certain anthocyanins -- including those found in chokeberry -- have also been shown to improve blood sugar and the function of insulin.
To better understand how chokeberries influence health, Drs. Bolin Qin and Richard Anderson from the US Department of Agriculture in Beltsville, MD studied what happens when prediabetic rats are fed chokeberry extracts for an extended period of time. The results of their research were presented on April 25 at the Experimental Biology 2010 meeting in Anaheim, CA. This presentation is part of the scientific program of the American Society for Nutrition, home of the world's leading nutrition researchers.
The researchers first made 18 male rats "prediabetic" or insulin insensitive by feeding them a fructose-rich diet for 6 weeks. Then they randomized the animals to continue drinking either pure water or water spiked with low or high levels of chokeberry extract (CellBerry®, Integrity Nutraceuticals International). After drinking this water for 6 weeks, the groups were compared in terms of body weight, body fat, blood glucose regulation, and molecular markers for inflammation.
Qin and Anderson found that at the end of the study the rats consuming the chokeberry-spiked water weighed less than the controls; both levels of chokeberry had the same effect in this regard. Similar beneficial effects of chokeberry consumption were found for body fat (specifically, that of the lower abdominal region). They also discovered that animals that had been drinking chokeberry extract had lower blood glucose and reduced levels of plasma triglycerides, cholesterol, and low-density lipoprotein (LDL) cholesterol when compared to the control animals. These alterations would theoretically lead to lower risk for diabetes and cardiovascular disease in humans. And to add even more evidence for a healthful impact of this super-berry, the researchers documented numerous alterations in expression of genes that would likely lead to reduced chronic inflammation and perhaps even lower cancer risk. For instance, drinking chokeberry extract lowered expression of the gene coding for interleukin-6 (IL-6), a protein that normally triggers inflammation following trauma or infection. Chronic overproduction of IL-6 has been documented in many diseases such as diabetes, arthritis, and atherosclerosis and is thought to be a partial cause of these conditions.
Of course, human studies will be needed before scientists can declare whether we derive the same health benefits from the chokeberry...
Saturday, April 24, 2010
Genetics in the Gut
Outnumbering our human cells by about 10 to one, the many minuscule microbes that live in and on our bodies are a big part of crucial everyday functions. The lion’s share live in the intestinal tract, where they help to fend off bad bacteria and aid in digestion. But as scientists determine what microbes are actually present and what they are doing, they are discovering that the bugs play an even larger role in human health than previously suspected—and perhaps at times exerting more influence than genes themselves.
A team that included Junjie Qin and Jun Wang of BGI-Shenzhen (formerly the Beijing Genomics Institute) completed a catalogue of some 3.3 million human gut microbe genes. The work, published in the March 4 Nature, adds to the expanding—but nowhere near complete—census of intestinal species. (Scientific American is part of Nature Publishing Group.)
The 3.3 million genes were a good deal “more than what we originally expected,” Wang says. The number was especially surprising given that the microbiota tended to be very similar across the 124 individuals the scientists sampled in Denmark and Spain. The team sequenced 576 billion base pairs, much larger than past work that found three billion base pairs. “These bacteria have functions that are essential to our health: they synthesize vitamins, break down certain compounds—which cannot be assimilated by our body—[and] play an important role in our immune system,” Wang points out.
Another group, led by Andrew Gewirtz of Emory University, turned its attention to a particular host gene that seems to affect these intestinal inhabitants. It found that in mice, a loss of one key gene led to a shift in microbiota communities and a rise in insulin resistance, obesity and other symptoms of so-called metabolic syndrome (a cluster of these conditions).
Gewirtz and his co-workers studied mice bred with the genetic deficiency: an absence of Toll-like receptor 5, or TLR5, which has a hand in immune response. They wanted to see how it might change microbial gut communities and metabolic health—and try to understand the order in which the changes were happening. “Obesity is associated with insulin resistance and type 2 diabetes,” Gewirtz says. But “which comes first is not entirely clear.”
As the researchers described in their paper published online March 4 by Science, they found that mice without the TLR5 gene—even when put on restricted diets—still showed insulin resistance, suggesting that the condition might lead to obesity rather than the other way around. But if these mice were allowed to eat as they pleased, they consumed 10 percent more than their peers and, by 20 weeks old, had body mass indexes that were 20 percent higher...
A team that included Junjie Qin and Jun Wang of BGI-Shenzhen (formerly the Beijing Genomics Institute) completed a catalogue of some 3.3 million human gut microbe genes. The work, published in the March 4 Nature, adds to the expanding—but nowhere near complete—census of intestinal species. (Scientific American is part of Nature Publishing Group.)
The 3.3 million genes were a good deal “more than what we originally expected,” Wang says. The number was especially surprising given that the microbiota tended to be very similar across the 124 individuals the scientists sampled in Denmark and Spain. The team sequenced 576 billion base pairs, much larger than past work that found three billion base pairs. “These bacteria have functions that are essential to our health: they synthesize vitamins, break down certain compounds—which cannot be assimilated by our body—[and] play an important role in our immune system,” Wang points out.
Another group, led by Andrew Gewirtz of Emory University, turned its attention to a particular host gene that seems to affect these intestinal inhabitants. It found that in mice, a loss of one key gene led to a shift in microbiota communities and a rise in insulin resistance, obesity and other symptoms of so-called metabolic syndrome (a cluster of these conditions).
Gewirtz and his co-workers studied mice bred with the genetic deficiency: an absence of Toll-like receptor 5, or TLR5, which has a hand in immune response. They wanted to see how it might change microbial gut communities and metabolic health—and try to understand the order in which the changes were happening. “Obesity is associated with insulin resistance and type 2 diabetes,” Gewirtz says. But “which comes first is not entirely clear.”
As the researchers described in their paper published online March 4 by Science, they found that mice without the TLR5 gene—even when put on restricted diets—still showed insulin resistance, suggesting that the condition might lead to obesity rather than the other way around. But if these mice were allowed to eat as they pleased, they consumed 10 percent more than their peers and, by 20 weeks old, had body mass indexes that were 20 percent higher...
Gene linking stress to obesity, diabetes discovered
Changes in the activity of a single gene in the brain can lead to metabolic changes that cause mice to develop symptoms associated with type 2 diabetes, as well as trigger anxious behavior.
These findings, discovered by Weizmann Institute of Science researchers, were published online this week in the Proceedings of the National Academy of Sciences (PNAS).
The constant stress many are exposed to in our modern society may thus be taking a heavy toll: Anxiety disorders and depression, as well as metabolic disorders such as obesity, type 2 diabetes and arteriosclerosis, have all been linked to stress.
These problems are reaching epidemic proportions. Type 2 diabetes alone is expected to affect some 360 million people around the world in 20 years.
The connection between stress, changes in appetite and anxiety-related behavior was recently proven scientifically, but the exact reasons for this were not clear until Dr. Alon Chen of the Rehovot institute’s neurobiology department and colleagues made their gene discovery.
They found that all the body’s systems are involved in the stress response, which evolved to deal with threats and danger. Behavioral changes tied to stress include heightened anxiety and concentration, while other changes in the body include heat-generation, changes in the metabolism of various substances and even changes in food preferences.
The Weizmann team suspected that a protein known as Urocortin-3 (Ucn3) was involved in tying all of these together. Produced in certain brain cells – especially in times of stress – it is known to play a role in regulating the body’s stress response.
These nerve cells have extensions that act as “highways” to speed Ucn3 on to two other sites in the brain: One, in the hypothalamus – the brain’s center for hormonal regulation of basic bodily functions – oversees, among other things, substance exchange and feelings of hunger and satiety; the other is involved in regulating behavior, including anxiety levels...
These findings, discovered by Weizmann Institute of Science researchers, were published online this week in the Proceedings of the National Academy of Sciences (PNAS).
The constant stress many are exposed to in our modern society may thus be taking a heavy toll: Anxiety disorders and depression, as well as metabolic disorders such as obesity, type 2 diabetes and arteriosclerosis, have all been linked to stress.
These problems are reaching epidemic proportions. Type 2 diabetes alone is expected to affect some 360 million people around the world in 20 years.
The connection between stress, changes in appetite and anxiety-related behavior was recently proven scientifically, but the exact reasons for this were not clear until Dr. Alon Chen of the Rehovot institute’s neurobiology department and colleagues made their gene discovery.
They found that all the body’s systems are involved in the stress response, which evolved to deal with threats and danger. Behavioral changes tied to stress include heightened anxiety and concentration, while other changes in the body include heat-generation, changes in the metabolism of various substances and even changes in food preferences.
The Weizmann team suspected that a protein known as Urocortin-3 (Ucn3) was involved in tying all of these together. Produced in certain brain cells – especially in times of stress – it is known to play a role in regulating the body’s stress response.
These nerve cells have extensions that act as “highways” to speed Ucn3 on to two other sites in the brain: One, in the hypothalamus – the brain’s center for hormonal regulation of basic bodily functions – oversees, among other things, substance exchange and feelings of hunger and satiety; the other is involved in regulating behavior, including anxiety levels...
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