According to a study published in The Journal of Clinical Endocrinology and Metabolism, researchers have found an association between low levels of a specific hormone and increased risk of metabolic disease in humans.
The study was conducted by Andrew Butler from the Florida campus of The Scripps Research Institute in collaboration with Peter J. Havel, professor of molecular biosciences and nutrition at the University of California, Davis.
The researchers focused on the hormone adropin, that had been previously identified by Butler's laboratory during an analysis of obese and insulin-resistant mice. Adropin is thought to play a vital role in controlling sugar levels and fatty acid metabolism.
Butler explained:
"The results of this clinical study suggest that low levels of adropin may be a factor increasing risk for developing metabolic disorders associated with obesity and insulin resistance, which could then lead to diseases such as type 2 diabetes."
Around 47 million adults in the U.S have metabolic syndrome, as stated by the American College of Cardiology. The National Institutes of Health defines metabolic syndrome as a group of risk factors, particularly obesity and insulin resistance, that occur alongside one another and increase the risk for developing coronary artery disease, stroke, and type 2 diabetes.
In the new study, which included 85 women and 45 men, the researchers demonstrated that obesity is linked with lower adropin levels. Lower adropin levels were additionally seen in people with a higher "metabolic syndrome risk factor" score, a score based on measuring triglycerides, LDL cholesterol, HDL, glucose, blood pressure, and waist circumference.
In addition, the team found circulating adropin concentrations dramatically increased at 3 and 6 months after gastric bypass surgery in patients who are morbidly obese. Remarkably, adropin levels reverted back to pre-surgical levels at 12 months after surgery.
Furthermore, the researchers found that in patients of normal weight, women had lower plasma adropin levels than men. Additionally, obesity had a greater adverse effect on adropin levels in men. According to the researchers, obesity in woman was also not connected with lower plasma adropin levels. The significance of the differences between men and woman is currently unknown.
Butler explained: "But the link between low levels of adropin and increased metabolic risk was observed in both sexes. The impact is there, irrespective of gender."
The team also discovered that adropin levels generally with age - the decline was greatest in people over Thirty years of age. Just like obesity, the aging effect seemed to be more evident in men.
The latest study is a crucial extension of previous pre-clinical studies using animal models published in the July edition of Obesity. In that study, the researchers removed the gene encoding adropin from mice and discovered that, while normal in appearance, adropin-deficient mice have insulin resistance and, when raised on high-fat diets, develop a more serious impaired glucose tolerance (IGT). These findings indicate decreased insulin production and attenuated response to insulin, which are the characterizing features of type 2 diabetes...
Sunday, August 19, 2012
Tuesday, July 10, 2012
Cutting Up Your Food May Help You Lose Weight
If you're looking to cut calories, you might start by cutting your food into smaller pieces. So suggests a study reported Tuesday in Zurich, Switzerland, at the international conference for the Society for the Study of Ingestive Behavior.
Arizona State University researchers gave 301 hungry college students either a whole bagel or the same bagel cut into four separate pieces. Twenty minutes later, both groups of students were treated to a free lunch.
What the researchers found was that the college students in both groups ended up eating roughly the same amount of each bagel; however the students that ate the bagel cut in four pieces ate roughly 25 percent less of their free lunch than the students who ate the uncut bagel.
The phenomenon appeared to hold true in animals as well. As part of the same study, the researchers also found that when hungry rats were given a choice to look for food either as a single large pellet or 30 small pellets, the rats ran faster and more frequently to the small pellets...
Arizona State University researchers gave 301 hungry college students either a whole bagel or the same bagel cut into four separate pieces. Twenty minutes later, both groups of students were treated to a free lunch.
What the researchers found was that the college students in both groups ended up eating roughly the same amount of each bagel; however the students that ate the bagel cut in four pieces ate roughly 25 percent less of their free lunch than the students who ate the uncut bagel.
The phenomenon appeared to hold true in animals as well. As part of the same study, the researchers also found that when hungry rats were given a choice to look for food either as a single large pellet or 30 small pellets, the rats ran faster and more frequently to the small pellets...
Binge Eating Improves With Deep Brain Stimulation Surgery
Deep brain stimulation reduces binge eating in mice, suggesting that this surgery, which is approved for treatment of certain neurologic and psychiatric disorders, may also be an effective therapy for obesity. Presentation of the results took place June 25 at The Endocrine Society's 94th Annual Meeting in Houston.
"Doing brain surgery for obesity treatment is a controversial idea," said the study's presenting author, Casey Halpern, MD, a fifth-year neurosurgery resident physician at the University of Pennsylvania, Philadelphia. "However, binge eating is a common feature of obese patients that frequently is associated with suboptimal treatment outcomes."
Currently the U.S. Food and Drug Administration has approved deep brain stimulation for use in various conditions that affect the brain, including Parkinson's disease and essential tremor. The procedure does not destroy any part of the brain and typically does not cause pain, Halpern said.
Available treatments of obesity may inadequately address the neural basis of this compulsive overeating behavior, he suggested. A region of the brain called the nucleus accumbens is known to be dysregulated in both rodents and people who binge eat. Therefore, Halpern and his co-workers targeted that brain region with deep brain stimulation in a strain of obesity-prone mice.
The surgery involved implanting an electrode in the nucleus accumbens. Wires connected the electrode to an external neurostimulator, a device similar to a pacemaker. When switched on, the stimulator triggers the electrode to deliver continuous electrical pulses to the brain.
After recovery from surgery, the mice received high-fat food at the same time every day for one hour, and the researchers measured their food consumption. Binge eating was defined as consuming 25 percent or more of the usual daily caloric intake during this period...
"Doing brain surgery for obesity treatment is a controversial idea," said the study's presenting author, Casey Halpern, MD, a fifth-year neurosurgery resident physician at the University of Pennsylvania, Philadelphia. "However, binge eating is a common feature of obese patients that frequently is associated with suboptimal treatment outcomes."
Currently the U.S. Food and Drug Administration has approved deep brain stimulation for use in various conditions that affect the brain, including Parkinson's disease and essential tremor. The procedure does not destroy any part of the brain and typically does not cause pain, Halpern said.
Available treatments of obesity may inadequately address the neural basis of this compulsive overeating behavior, he suggested. A region of the brain called the nucleus accumbens is known to be dysregulated in both rodents and people who binge eat. Therefore, Halpern and his co-workers targeted that brain region with deep brain stimulation in a strain of obesity-prone mice.
The surgery involved implanting an electrode in the nucleus accumbens. Wires connected the electrode to an external neurostimulator, a device similar to a pacemaker. When switched on, the stimulator triggers the electrode to deliver continuous electrical pulses to the brain.
After recovery from surgery, the mice received high-fat food at the same time every day for one hour, and the researchers measured their food consumption. Binge eating was defined as consuming 25 percent or more of the usual daily caloric intake during this period...
Why Do Fat Cells Get Fat? New Suspect Identified
As the world fights obesity at the human level, scientists at the University of Michigan and their colleagues have made a surprising finding at the microscopic level that could help fuel that fight.
Their work helps explain why fat-storing cells get fatter, and burn fat slower, as obesity sets in. If their findings from mice can be shown to apply to humans, they may provide a new target for obesity-fighting drugs.
By studying the tiny signals that fat-storing cells send to one another, the team has shown a crucial and previously unknown role for a molecule called Sfrp5.
The results, which appear online June 25 and will be in the July issue of the Journal of Clinical Investigation, surprised them.
In a series of experiments, the team showed that Sfrp5 influences a signaling pathway known as WNT to stimulate fat cells -- called adipocytes -- to grow larger and to suppress the rate at which fat is burned in the mitochondria inside them.
By stopping cells from making Sfrp5, they were able to make mice that didn't get as fat as quickly because their adipocytes didn't grow large -- even when the mice were fed a high-fat diet. They even showed the impact when transplanting fat from Sfrp5 -- deficient mice into other mice...
Their work helps explain why fat-storing cells get fatter, and burn fat slower, as obesity sets in. If their findings from mice can be shown to apply to humans, they may provide a new target for obesity-fighting drugs.
By studying the tiny signals that fat-storing cells send to one another, the team has shown a crucial and previously unknown role for a molecule called Sfrp5.
The results, which appear online June 25 and will be in the July issue of the Journal of Clinical Investigation, surprised them.
In a series of experiments, the team showed that Sfrp5 influences a signaling pathway known as WNT to stimulate fat cells -- called adipocytes -- to grow larger and to suppress the rate at which fat is burned in the mitochondria inside them.
By stopping cells from making Sfrp5, they were able to make mice that didn't get as fat as quickly because their adipocytes didn't grow large -- even when the mice were fed a high-fat diet. They even showed the impact when transplanting fat from Sfrp5 -- deficient mice into other mice...
Scientists Identify Target for Obesity and Atherosclerosis
Scientists claim that an enzyme already implicated in the control of tumorigenesis through p53 activation may also directly act to control obesity and atherosclerosis. Wip1 phosphatase is a known negative regulator of ataxia telangiectasia mutated (Atm)-dependent signaling, and knocking out the Wip1 gene, which is amplified in a range of primary human cancers, has been shown to result in tumor resistance in a number of cancer-prone mouse models. Dmitry V. Bulavin, Ph.D., at the Institute of Molecular and Cell Biology and the Singapore Bioimaging Consortium (SBIC) have now found that Wip1 deficiency also makes mice resistant to diet-induced obesity and prevents the development of atherosclerosis in ApoE-knockout animals.
Their findings, reported in Cell Metabolism, indicate that Wip1’s role in controlling obesity and atherosclerosis is dependent on an Atm-mTOR signaling pathway that doesn’t involve p53. Instead, knocking out Wip1 prevents the accumulation of lipid droplets in macrophages and their conversion into foam cells through increased autophagy. Dr Bulavin, et al’s published paper is titled “Wip1-Dependent Regulation of Autophagy, Obesity, and Atherosclerosis.”
Atherosclerosis starts to develop when low-density lipoprotein (LDL) is oxidised by free radicals to generate oxLDL, which damages arterial walls and triggers repair mechanisms. The repair process involves the recruitment of monocytes to the damaged arterial walls, and their differentiation into macrophages that ingest oxLDL and accumulate cholesterol in the form of lipid droplets, leading to the formation of foam cells. Because the cells can’t process the oxLDL, they continue to grow and eventually rupture, depositing even more oxidized cholesterol in the arterial wall, and propagating further immune responses.
Studies by the Singapore team in engineered mice now suggest that Wip1 phosphatase promotes atherosclerosis, as well as diet-induced weight gain and fat accumulation. They found that genetic-knockout animals lacking ApoE and Wip1 put on far less weight when fed a high-fat western diet than ApoE knockouts that retained wild-type Wip1. In comparison with the wild-type Wip1 animals, the double knockouts had far less body fat and lighter livers with evidence of suppressed steatosis. They also ate less and expended more energy. Importantly, the ApoE/Wip1 knockout mice demonstrated higher usage of fat as an energy source...
Their findings, reported in Cell Metabolism, indicate that Wip1’s role in controlling obesity and atherosclerosis is dependent on an Atm-mTOR signaling pathway that doesn’t involve p53. Instead, knocking out Wip1 prevents the accumulation of lipid droplets in macrophages and their conversion into foam cells through increased autophagy. Dr Bulavin, et al’s published paper is titled “Wip1-Dependent Regulation of Autophagy, Obesity, and Atherosclerosis.”
Atherosclerosis starts to develop when low-density lipoprotein (LDL) is oxidised by free radicals to generate oxLDL, which damages arterial walls and triggers repair mechanisms. The repair process involves the recruitment of monocytes to the damaged arterial walls, and their differentiation into macrophages that ingest oxLDL and accumulate cholesterol in the form of lipid droplets, leading to the formation of foam cells. Because the cells can’t process the oxLDL, they continue to grow and eventually rupture, depositing even more oxidized cholesterol in the arterial wall, and propagating further immune responses.
Studies by the Singapore team in engineered mice now suggest that Wip1 phosphatase promotes atherosclerosis, as well as diet-induced weight gain and fat accumulation. They found that genetic-knockout animals lacking ApoE and Wip1 put on far less weight when fed a high-fat western diet than ApoE knockouts that retained wild-type Wip1. In comparison with the wild-type Wip1 animals, the double knockouts had far less body fat and lighter livers with evidence of suppressed steatosis. They also ate less and expended more energy. Importantly, the ApoE/Wip1 knockout mice demonstrated higher usage of fat as an energy source...
Fat Fighting Is Part of the Apple's Peel
Eating unpeeled apples may keep extra pounds and obesity-related diseases at bay, a study in PLoS ONE suggests.
Ursolic acid is a natural compound found in the waxy coats on apples and other fruits and herbs. Previous research showed that ursolic acid increased the activity of a protein that stimulated muscle growth and glucose metabolism in mice.
Ursolic acid, found in apples' waxy coats, triggered an increase in high-energy brown fat, which is associated with reduced obesity, in mice in an Iowa study.
In this follow-up study, researchers in Iowa tested ursolic acid on mice with diet-induced obesity. For six weeks, one group of mice had unlimited access to a diet of high-fat food proven to cause obesity, glucose intolerance and fatty liver disease. Two other groups of mice had unlimited access to the same diet, but supplemented with either 0.14 grams or 0.27 grams of ursolic acid per 100 grams of food. For comparison, an apple contains 50 milligrams of ursolic acid, equivalent to about 6% of the lowest dose given to the mice.
Ursolic-acid mice developed more skeletal muscle but gained less weight than nonsupplemented mice, even though food intake was higher in ursolic-acid mice. Supplemented mice had greater strength and exercise capacity, and higher resting energy expenditure. Ursolic acid triggered an increase in high-energy brown fat associated with reduced obesity, though it isn't known how, researchers said. The results were the same for both ursolic-acid doses...
Ursolic acid is a natural compound found in the waxy coats on apples and other fruits and herbs. Previous research showed that ursolic acid increased the activity of a protein that stimulated muscle growth and glucose metabolism in mice.
Ursolic acid, found in apples' waxy coats, triggered an increase in high-energy brown fat, which is associated with reduced obesity, in mice in an Iowa study.
In this follow-up study, researchers in Iowa tested ursolic acid on mice with diet-induced obesity. For six weeks, one group of mice had unlimited access to a diet of high-fat food proven to cause obesity, glucose intolerance and fatty liver disease. Two other groups of mice had unlimited access to the same diet, but supplemented with either 0.14 grams or 0.27 grams of ursolic acid per 100 grams of food. For comparison, an apple contains 50 milligrams of ursolic acid, equivalent to about 6% of the lowest dose given to the mice.
Ursolic-acid mice developed more skeletal muscle but gained less weight than nonsupplemented mice, even though food intake was higher in ursolic-acid mice. Supplemented mice had greater strength and exercise capacity, and higher resting energy expenditure. Ursolic acid triggered an increase in high-energy brown fat associated with reduced obesity, though it isn't known how, researchers said. The results were the same for both ursolic-acid doses...
Obesity Vaccine Effective In Mice
New vaccines promote weight loss. A new study, published in BioMed Central's open access journal, Journal of Animal Science and Biotechnology, assesses the effectiveness of two somatostatin vaccinations, JH17 and JH18, in reducing weight gain and increasing weight loss in mice.
Obesity and obesity-related disease is a growing health issue worldwide. Somatostatin, a peptide hormone, inhibits the action of growth hormone (GH) and insulin-like growth factor (IGF-1), both of which increase metabolism and result in weight loss. Vaccination with modified somatostatin causes the body to generate antibodies to somatostatin, effectively removing this inhibition without directly interfering with the growth hormones and subsequently increasing energy expenditure and weight loss.
Keith Haffer from Braasch Biotech LLC, tested the vaccinations in two groups of ten diet-induced obese male mice compared with a control group of ten mice which received saline injections. Mice in all groups had been fed a high fat diet for eight weeks prior to the study and continued to eat the same food for the duration of the six-week study. The vaccinations were administered twice - at the start of the study followed by a booster vaccination on day 22.
Four days after the first injection of modified somatostatin, the vaccinated mice had a 10% drop in body weight (not seen in the control mice). At the end of the study, results showed that both vaccines induced antibodies to somatostatin and significantly reduced body weight, sustaining a 10% lower body weight, without affecting normal levels of the growth hormone IGF-1, or insulin levels...
Obesity and obesity-related disease is a growing health issue worldwide. Somatostatin, a peptide hormone, inhibits the action of growth hormone (GH) and insulin-like growth factor (IGF-1), both of which increase metabolism and result in weight loss. Vaccination with modified somatostatin causes the body to generate antibodies to somatostatin, effectively removing this inhibition without directly interfering with the growth hormones and subsequently increasing energy expenditure and weight loss.
Keith Haffer from Braasch Biotech LLC, tested the vaccinations in two groups of ten diet-induced obese male mice compared with a control group of ten mice which received saline injections. Mice in all groups had been fed a high fat diet for eight weeks prior to the study and continued to eat the same food for the duration of the six-week study. The vaccinations were administered twice - at the start of the study followed by a booster vaccination on day 22.
Four days after the first injection of modified somatostatin, the vaccinated mice had a 10% drop in body weight (not seen in the control mice). At the end of the study, results showed that both vaccines induced antibodies to somatostatin and significantly reduced body weight, sustaining a 10% lower body weight, without affecting normal levels of the growth hormone IGF-1, or insulin levels...
Sunday, June 24, 2012
Apple Peel Compound Boosts Brown Fat, Reduces Obesity in Mice
Obesity and its associated problems such as diabetes and fatty liver disease are increasingly common global health concerns. A new study by University of Iowa researchers shows that a natural substance found in apple peel can partially protect mice from obesity and some of its harmful effects.
The findings suggest that the substance known as ursolic acid reduces obesity and its associated health problems by increasing the amount of muscle and brown fat, two tissues recognized for their calorie-burning properties.
The study, which was published June 20 in the journal PLoS ONE, was led by Christopher Adams, M.D., Ph.D., UI associate professor of internal medicine and a Faculty Scholar at the Fraternal Order of Eagles Diabetes Research Center at the UI.
"From previous work, we knew that ursolic acid increases muscle mass and strength in healthy mice, which is important because it might suggest a potential therapy for muscle wasting," Adams says. "In this study, we tested ursolic acid in mice on a high-fat diet -- a mouse model of obesity and metabolic syndrome. Once again, ursolic acid increased skeletal muscle. Interestingly, it also reduced obesity, pre-diabetes and fatty liver disease.
"Since muscle is very good at burning calories, the increased muscle in ursolic acid-treated mice may be sufficient to explain how ursolic acid reduces obesity. However, we were surprised to find that ursolic acid also increased brown fat, a fantastic calorie burner. This increase in brown fat may also help protect against obesity."
Until quite recently, researchers believed that only infants had brown fat, which then disappeared during childhood. However, improved imaging techniques have shown that adults do retain a very small amount of the substance mostly in the neck and between the shoulder blades. Some studies have linked increased levels of brown fat with lower levels of obesity and healthier levels of blood sugar and blood lipid, leading to the suggestion that brown fat may be helpful in preventing obesity and diabetes...
The findings suggest that the substance known as ursolic acid reduces obesity and its associated health problems by increasing the amount of muscle and brown fat, two tissues recognized for their calorie-burning properties.
The study, which was published June 20 in the journal PLoS ONE, was led by Christopher Adams, M.D., Ph.D., UI associate professor of internal medicine and a Faculty Scholar at the Fraternal Order of Eagles Diabetes Research Center at the UI.
"From previous work, we knew that ursolic acid increases muscle mass and strength in healthy mice, which is important because it might suggest a potential therapy for muscle wasting," Adams says. "In this study, we tested ursolic acid in mice on a high-fat diet -- a mouse model of obesity and metabolic syndrome. Once again, ursolic acid increased skeletal muscle. Interestingly, it also reduced obesity, pre-diabetes and fatty liver disease.
"Since muscle is very good at burning calories, the increased muscle in ursolic acid-treated mice may be sufficient to explain how ursolic acid reduces obesity. However, we were surprised to find that ursolic acid also increased brown fat, a fantastic calorie burner. This increase in brown fat may also help protect against obesity."
Until quite recently, researchers believed that only infants had brown fat, which then disappeared during childhood. However, improved imaging techniques have shown that adults do retain a very small amount of the substance mostly in the neck and between the shoulder blades. Some studies have linked increased levels of brown fat with lower levels of obesity and healthier levels of blood sugar and blood lipid, leading to the suggestion that brown fat may be helpful in preventing obesity and diabetes...
Take your exercise pill
Scientists may be able to come up with a pill that makes you want to exercise, thus solving -- sort of -- the nation's obesity epidemic. Swiss researchers have found that by elevating a hormone --erythropoietin (Epo) -- in mice, they were more motivated to exercise. To make this discovery, Gassmann and colleagues used three types of mice: those that received no treatment, those that were injected with human Epo, and those that were genetically modified to produce human Epo in the brain. Compared to the mice that did not have any increase in Epo, both mouse groups harboring human Epo in the brain showed significantly higher running performance without increases in red blood cells. "If you can't put exercise in a pill, then maybe you can put the motivation to exercise in a pill instead," said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. "As more and more people become overweight and obese, we must attack the problem from all angles. Maybe the day will come when gyms are as easily found as fast food restaurants."...
Tree oil may combat obesity, diabetes, S&T research suggests
A future weapon in the battle against obesity and diabetes could come in the form of an oil derived from the seeds of wild almond trees, according to researchers at Missouri University of Science and Technology. The key to the oil's potential lies in its ability to affect certain microorganisms living in our bellies. In a study presented today (Monday, June 18, 2012) at the American Society for Microbiology's general meeting in San Francisco, Missouri S&T researchers reported that adding sterculic oil to the diets of obese laboratory mice increased their sensitivity to insulin. This was due to the oil's effect on three types of microorganisms that live in the guts of the mice...
Higher dose of milk vitamin fights obesity
A novel form of vitamin B3 in milk given in a high dose to mice fed a fatty diet seemed to help prevent obesity, U.S. and Swiss researchers said.
Dr. Anthony Sauve of Weill Cornell Medical College in New York and Dr. Johan Auwerx of Federal Polytechnic School in Lausanne, Switzerland, said high doses of the vitamin precursor, nicotinamide riboside -- a cousin of niacin -- prevented obesity in mice fed a fatty diet and also increased muscle performance, improved energy expenditure and prevented diabetes development, all without side effects. This form of vitamin B3 is found in milk in small quantities...
Sunday, June 10, 2012
Fat-busting, super diet pill could help beat obesity by preventing those hunger pangs
A super diet pill aimed at curbing fat people's appetites could soon be a reality thanks to boffins who have found the secret to tackling obesity may lie in the brain.
The pill would not only shrink waist lines but also the £4.2 billion NHS bill for treating obesity related illness such as cancer, diabetes and heart disease.
Scientists in the US believe the hypothalmus area of the brain - a receptor controlling body temperature, hunger, thirst and fatigue - is particularly sensitive to drugs which could hold the key to fighting flab.
Professor Domenico Accili, from Columbia University Medical Center, said: 'We've identified a receptor that is immediately involved in regulating food intake.
'What is especially encouraging is that it is a highly 'druggable' target. In fact, several existing medications already seem to interact with this receptor.'
The researchers, whose findings are published in the Cell journal, studied insulin and leptin hormones, which inhabit the AgRP molecule and are vital to maintaining the body's energy balance.
They did so by creating a strain of mice to explore the effects of appetite stimulation and discovered a gene called Gpr17.
The scientists found that when the gene was injected into normal rodents, it resulted in an increase in appetite and a decrease when it was blocked - without negative side effects...
The miracle molecule: Hidden vitamin found in BEER and MILK can make you stronger, slimmer and healthier
If you were planning on having a quick pint tonight, then this will be welcome news.
Beer may contain a vitamin which can fight obesity and improve muscle strength, scientists claim.
The ‘miracle molecule’, which has been found in milk and may also be present in beer and some foods, has no side effects and could even lengthen lifespan, they say.
The snag is that the molecule, called nicotinamide riboside (NR), is extremely small, difficult to find and expensive to synthesise.
Johnan Auwerx, head of the Ecole Polytechnique Federale in Lausanne, Switzerland, said experiments using mice revealed the molecule’s potential.
In an article in the specialist journal Cell Metabolism journal, Mr Auwerx called the results 'impressive'
'NR appears to play a role in preventing obesity,' said Mr Auwerx.
Working with Weill Cornell Medical College in New York, his team found mice on a high-fat diet that were fed NR gained significantly less weight – 60 per cent – than mice eating the same diet without NR supplements.
And none of the NR-treated mice had indications that they were developing diabetes, unlike the untreated mice.
Mice which were fed NR supplements over a ten-week period had better endurance performance than those who were not...
Improving obesity-induced insulin sensitivity
In recent years, a growing body of evidence has linked inflammation to the development of insulin resistance. In insulin resistance, the hormone insulin is less effective in promoting glucose uptake from the bloodstream into other tissues. Obesity is a major factor that contributes to insulin resistance, which can eventually lead to type 2 diabetes. Previous studies have shown that proinflammatory molecules found in fat tissue decreases sensitivity of tissues to insulin.
To identify drug targets that will improve insulin sensitivity, Dr. Jerrold Olefsky and colleagues from the University of California in San Diego investigated the role of G protein-coupled receptor 21 (GPR21) in insulin resistance and energy homeostasis. The group compared mice without the gene encoding GPR21 to healthy control mice under normal and high-fat diet conditions. They discovered that mice lacking GPR21 had enhanced insulin sensitivity and increased energy expenditure independent of diet. This result was attributed to the reduced migration of inflammatory cells to the liver and fat tissue in the absence GPR21. Under normal diet, absence of GPR21 in the hypothalamus caused a modest decrease in body weight. This is the first study to demonstrate the negative impact of GPR21 on inflammation and insulin sensitivity. Their findings suggest that GPR21 inhibition may improve insulin resistance and enhance energy expenditure, making GPR21 inhibitors promising treatments for diabetes.
Is There a 'Healthy' Obesity Gene?
Why is it that some obese people are healthier than others? This was one of the main questions Dr. Chaodong Wu of the College of Agriculture and Life Sciences -- Texas A&M University System -- and a group of researchers tried to answer in a recent study.
The study, which will appear in a July issue of the Journal of Biological Chemistry, used genetically modified mice to investigate the genetic aspects of why some obese people do not develop certain medical problems typically associated with obesity, especially Type 2 diabetes.
Wu noted that Xin Guo, a Ph.D. candidate in the college's department of nutrition and food sciences, contributed significantly to the study.
"Previous research had indicated that a regulatory enzyme which is encoded by the gene PFKFB3 protects against diet-induced fat tissue inflammation and systemic insulin resistance," said Wu, who also has a Texas AgriLife Research appointment. "Increasing evidence shows that fat deposition, or amount, is not directly associated with the inflammation or insulin resistance in the development of obesity-related metabolic diseases."
Wu said the inducible 6-phosphorofructo-2-kinase (iPFK2) enzyme links metabolic and inflammatory responses and may underlie what he refers to as "healthy" obesity.
"While many obese people develop Type 2 diabetes, heart conditions and other chronic health problems associated with being significantly overweight, other obese people do not," he said. "And while obesity in general is not healthy, some obese people do not develop the diseases more commonly associated with a less-than-healthy diet. Furthermore, a number of thinner people may have the sort of health problems more typically associated with obesity."
Wu said he and the other researchers theorized that these diseases are associated with the cellular inflammatory response brought on by obesity.
"We also thought this gene could conceivably be targeted for use in the treatment of diabetes, especially Type 2, commonly associated with obesity," he said. "We wanted to find out what might happen to a subject if that particular gene was activated."
Wu and his fellow researchers used laboratory mice to explore the effect of a targeted adipocyte overexpression of the gene/enzyme combination on diet-induced inflammatory responses and insulin sensitivity...
Timing of meals is tied to obesity
Gaining weight is not just the result of the number of calories eaten but also may have to do with the time of day those calories are consumed, at least in mice.
The researchers, from the Salk Institute in California and elsewhere, fed the mice a high-fat diet or a standard diet. Some of the mice were allowed to eat only within an eight-hour period each day and the others were given an unrestricted amount of time to eat.
When mice on the high-fat diet were restricted to eating within eight hours, they consumed just as much as those on the same diet who were permitted to eat around the clock. However, the mice with unrestricted eating times were more likely to become obese or have other metabolic disorders.
Monday, May 21, 2012
Gut Organisms Could Be Clue in Controlling Obesity Risk
The international obesity epidemic is widespread, nondiscriminatory, and deadly. But do we really understand all of the factors underlying this alarming trend? The concept of energy balance (energy consumed = energy expended + energy stored) is undeniable, being driven by the first law of thermodynamics. Consequently, there is no contradiction that excessive calorie intake and plummeting levels of physical activity are largely to blame for our ever-expanding waistlines.
However, scientists remain baffled as to why some individuals are particularly prone to becoming obese and if there is anything aside from lowering calorie consumption and increasing activity levels that can be done to prevent and/or reverse excessive weight gain in our most at-risk populations.
Physiologists have long known that our intestines are brimming with live bacteria, some of which provide important substances (e.g., vitamin B-12) to their host. However, research conducted over the last decade suggests that these organisms, often referred to as intestinal microbiota, may play a far greater role in human health than previously imagined. One area of intense interest is the possibility that the mix of intestinal bacteria with which we are endowed might directly influence our risk for obesity. Obese individuals tend to have different microbial profiles in their intestines than lean individuals, and scientists have learned that the bacteria common to obesity may metabolize the food we eat in a way that allows us to harvest more calories from it and deposit those calories as fat.
To determine whether altering one's bacterial profile can change obesity risk, researchers from the French Institute for Agricultural Research (INRA) transferred the intestinal bacteria of obesity-prone or obesity-resistant rats into the intestinal tracts of germ-free mice recipients, therefore having no innate gut microbiota. Some animals were fed a regular diet, whereas others were provided unlimited access to a high-fat diet. Food intake and weight gain were monitored for 8 weeks, and intestinal samples were analyzed for a variety of physiologic markers of metabolism and normal feedback mechanisms known to play a role in maintenance of energy balance.
As hypothesized, mice that received intestinal bacteria from obesity-prone animals ate more food, gained more weight, and became more obese than those receiving microbiota from obesity-resistant animals. Animals with microbiota transferred from obesity-prone animals also exhibited changes in intestinal nutrient sensors and gut peptide levels, likely influencing how the animals responded to eating.
The authors' conclusions are three-fold. First, they theorize that obese individuals, when given the opportunity to overeat, may harbor specific gut microbiota profiles that promote excess weight gain. Second, they propose that differences in gut microbes can be related to behavioral changes and increased food intake. Finally, they believe that the mix of microbiota you have may influence your ability to properly sense and respond to a meal. They hope to eventually find ways to manipulate the intestinal microbiota profiles of especially at-risk individuals so that they can more easily maintain a healthy body weight...more
Men with low testosterone face increased risk of obesity and diabetes
MEN with low levels of testosterone could be at greater risk of developing diabetes, a study has suggested.
Researchers from Edinburgh University found low testosterone levels are linked to a resistance to insulin, the hormone that controls blood sugar levels.
• Research shows low testosterone levels “instrumental” in onset of diabetes
• Men with low levels of testosterone are more likely to become obese
Testosterone is present throughout the body and low levels are associated with increased obesity, a known risk factor for developing type 2 diabetes.
But scientists said the study provides evidence of increased risk “even when body mass is not affected”.
Dr Kerry McInnes, from the university’s endocrinology unit, said: “We know that men with low testosterone levels are more likely to become obese and as a result, develop diabetes.
“This study shows that low testosterone is a risk factor for diabetes no matter how much a person weighs. As men age, their testosterone levels lower. This, along with increasing obesity, will increase the incidence of diabetes.”
The research team said the study is the first to directly show how low testosterone levels in fat tissue can be “instrumental” in the onset of the condition.
They said the findings show that mice with impaired testosterone function in fat tissue were more likely to be insulin-resistant. However, they also reveal that insulin resistance occurs in mice when testosterone function was impaired regardless of body weight...more
Sunday, May 20, 2012
Nighttime fasting may foster weight loss
In an age of long commutes, late sports practices, endless workdays and 24/7 television programming, the image of Mom hanging up her dish towel at 7 p.m. and declaring "the kitchen is closed" seems a quaint relic of an earlier era.
It also harks back to a thinner America. And that may be no coincidence.
A new study, conducted on mice, hints at an unexpected contributor to the nation's epidemic of obesity — and, if later human studies bear it out, a possible way to have our cake and eat it too, with less risk of weight gain and the diseases that come with it...more
Saturday, April 28, 2012
Manipulating Molecules in Heart Protects Mice On High-Fat Diets from Obesity, Affects Metabolism
UT Southwestern Medical Center researchers have demonstrated for the first time that the heart can regulate energy balance throughout the body, a finding that may point to more effective treatments for obesity, diabetes, and heart disease.
Obesity, cardiovascular disease, and diabetes affect tens of millions of people in the U.S., according to the Centers for Disease Control and Prevention.
Using mice fed a high-fat diet, researchers found that manipulating a heart-specific genetic pathway prevents obesity and protects against harmful blood-sugar changes associated with type 2 diabetes...more
Sunday, April 15, 2012
Fat gene may predict protection against diabetes, study suggests
While obesity is a huge risk factor for type 2 diabetes, many people with 50 or 60 extra pounds to lose never develop the condition, and a new study from Beth Israel Deaconess Medical Center provides a possible explanation. It may have something to do with how much they express a particular gene in their fat cells; the gene makes cells more sensitive to the hormone insulin which transports glucose into cells.
Normally, type 2 diabetes occurs when cells become resistant to insulin, causing blood sugar levels to rise to dangerously high levels. In the study published Sunday in the journal Nature, the researchers manipulated the “glucose transporter” gene in obese mice to allow more sugar into fat cells and found that the mice didn’t develop diabetes. On the flip side, normal weight mice who lacked the glucose transporter gene had soaring blood sugar levels.
“We all have this gene but how much it’s turned on and expressed in our fat cells seems to be predictive of how metabolically healthy we are,” explained study co-author Dr. Barbara Kahn, an endocrinologist at Beth Israel Deaconess Medical Center. Those with high levels of expression get more protection from diabetes, while those with low levels have less protection...
New lab mice cut search for genetic links to disease by more than a decade
With a 95 percent genomic similarity to humans, mice have long been used to learn about the genetic causes of human disease. Once researchers can shine a light on the genetic factors that cause disease in mice, they can start to develop prevention and treatment options to protect the human population.
But this process, called genetic mapping, is a long and difficult road, made more challenging by the 5% difference between the humans and lab mice. Now Prof. Fuad Iraqi of Tel Aviv University's Sackler Faculty of Medicine is closing the gap with an international project called Collaborative Cross. The project is developing lab mice with increased genetic diversity, making them more advantageous for genetic research related to human health.
The new population will offer 1,000 genetic strains within a fixed genotype — the composite of the entire genetic makeup of an organism. This is a marked improvement on the previously existing 450 genetic strains of lab mice with varying genotypes, making Prof. Iraqi's new strain ideal for genetic mapping. And with these mice, researchers will be able to identify a gene associated with a particular disease within two to three years instead of the 10 to 15 years it takes now, says Prof. Iraqi...
Biologist claims certain chemicals increase chance of obesity
Obesity is at epidemic proportions in this country.
But what if some people are overweight, not only because of the brownies they eat, but because of the plastic containers they store them in?
The conventional theory goes that people become obese because they take in more calories than they burn off. But molecular biologist Bruce Blumberg says it’s more complicated than that.
"If it were a simple problem, a matter of balancing our caloric checkbook, no one would be fat," says Blumberg. "We are not a country full of lazy people who just eat everything in sight."
In his lab at UC Irvine, some of his mice are obese. Blumberg made them that way, but not by overfeeding them.
"My mice become fatter on a normal diet," Blumberg explains. "That’s only because they were exposed to this chemical in the womb."
The chemical he’s talking about is called Tributyltin. It’s used to preserve wood and is found in some vinyl products. There are more than a dozen kinds of drugs and chemicals that make lab animals — or people — fat. Blumberg calls them obesogens...
Fat mice provide genetic clues to obesity puzzle
A new study published in Nature Medicine provides clues as to how a gene mutation may lead to obesity.
Mutations in the brain-derived neurotrophic factor gene (BDNF) have previously been shown to cause obesity in mice and have been identified in severely obese children. Genome-wide association studies have also confirmed BDNF as a susceptibility gene for common obesity in humans.
The study investigated the mechanism by which BDNF mutations lead to obesity. Obesity is caused by an excess of energy, which can result from high energy intake, low energy expenditure, or both. Obesity was caused solely by overeating in mice with BDNF mutations, which consumed up to 80% more food than those without the mutation (‘wild type’ mice). When the mice with the mutation were restricted to the amount of food that that the wild type mice chose to eat, they did not become obese...
Study has shown to reverse obesity, body fat and improve insulin sensitivity in mice
Scientists used the ACE inhibitor captopril (CAP)—commonly used for the treatment of hypertension and cardiac conditions—and found that it can reduce the body weight of mice maintained on a high-fat diet.
Initially, mice were put on a high fat diet for 12 weeks to produce mice with diet-induced obesity. During the subsequent 12 weeks treatment period, the mice were allowed access to the high-fat diet and either water containing CAP or plain tap water (the control).
"From the first week of treatment, food intake and body weight decreased in the mice treated with CAP compared with the control mice.
"Both peripheral insulin sensitivity and hepatic insulin sensitivity were improved in CAP treated mice compared with the control, which means there was an improvement in the handling of blood sugar," says Dr. Shirmila Premaratna, lead researcher from the La Trobe’s Faculty of Science, Technology and Engineering...
Sunday, April 01, 2012
Skinny genes – how GM food may help you stave off obesity
Fond of a full English breakfast? Perhaps you should have a glass of blood orange juice on the side – it might help to reduce the harm from all the fat you are ingesting, and make you less likely to become obese.
But as blood oranges are among the least favoured fruits for consumers, scientists in the UK are hoping to find ways to genetically modify standard oranges to incorporate the beneficial effects of their less popular cousins.
The project is one of several aimed at improving health through the genetic modification of plants – a process that scientists say could be a low-cost answer to harmful nutritional deficiencies.
Another project involves incorporating algae genes into oilseed rape, in order to produce nutritionally vital fish oils without having to kill fish; and grains modified to take up more zinc from the environment, to alleviate the zinc deficiency that blights millions.
The scientists involved believe that the public will be more accepting of GM plants that plug common nutritional gaps, than those crops that benefit big companies. "This isn't about increasing the profits from multinationals – there are big gains to be had," said Prof Dale Sanders, director of the John Innes Centre, an independent centre for plant science and microbiology research.
Although only a handful of GM experiments are licensed in the UK at present, some lab research continues, although scientists are concerned that the science is moving elsewhere. Cathie Martin, also of the John Innes Centre, who is leading the research on blood oranges, said: "There are enormous problems in creating something that can be grown in Europe, and big problems in public funding, because of the regulation."
Unpublished research has suggested that compounds found within blood oranges could help to cut obesity by reducing the accumulation of fats, and so avoid some of the harm from fatty foods. In one human study, people fed a full English breakfast along with the juice of three blood oranges experienced less accumulation of fat, possibly because of substances known as anthocyanins, found in abundance in blood oranges.
The results should be taken with caution – they are unpublished and have not yet been peer-reviewed. Studies on mice have shown a similar effect, preventing obesity in mice fed a high-fat diet, compared to mice given ordinary orange juice, or water, but the human effects are still uncertain...
But as blood oranges are among the least favoured fruits for consumers, scientists in the UK are hoping to find ways to genetically modify standard oranges to incorporate the beneficial effects of their less popular cousins.
The project is one of several aimed at improving health through the genetic modification of plants – a process that scientists say could be a low-cost answer to harmful nutritional deficiencies.
Another project involves incorporating algae genes into oilseed rape, in order to produce nutritionally vital fish oils without having to kill fish; and grains modified to take up more zinc from the environment, to alleviate the zinc deficiency that blights millions.
The scientists involved believe that the public will be more accepting of GM plants that plug common nutritional gaps, than those crops that benefit big companies. "This isn't about increasing the profits from multinationals – there are big gains to be had," said Prof Dale Sanders, director of the John Innes Centre, an independent centre for plant science and microbiology research.
Although only a handful of GM experiments are licensed in the UK at present, some lab research continues, although scientists are concerned that the science is moving elsewhere. Cathie Martin, also of the John Innes Centre, who is leading the research on blood oranges, said: "There are enormous problems in creating something that can be grown in Europe, and big problems in public funding, because of the regulation."
Unpublished research has suggested that compounds found within blood oranges could help to cut obesity by reducing the accumulation of fats, and so avoid some of the harm from fatty foods. In one human study, people fed a full English breakfast along with the juice of three blood oranges experienced less accumulation of fat, possibly because of substances known as anthocyanins, found in abundance in blood oranges.
The results should be taken with caution – they are unpublished and have not yet been peer-reviewed. Studies on mice have shown a similar effect, preventing obesity in mice fed a high-fat diet, compared to mice given ordinary orange juice, or water, but the human effects are still uncertain...
'Gluttony gene' stops mice feeling full
A mutation in a gene linked to obesity causes mice to eat up to 80 percent more than normal, a study suggests.
After eating, hormones send signals to the brain to let it know it's full. However, scientists found that in mice with a faulty version of the BDNF gene, these messages were 'blocked'.
'If there is a problem with the BDNF gene, neurons can't talk to each other, and the leptin and insulin [hormone] signals are ineffective, and appetite is not modified', said researcher Professor Baoji Xu from the Georgetown Medical Centre in the USA.
When the team monitored the eating habits of mice with and without the mutation, they found males were twice as heavy as their normal counterparts, and females were 2.7 times heavier. This was to do with them over-eating, rather than a reduction in their activity levels...
After eating, hormones send signals to the brain to let it know it's full. However, scientists found that in mice with a faulty version of the BDNF gene, these messages were 'blocked'.
'If there is a problem with the BDNF gene, neurons can't talk to each other, and the leptin and insulin [hormone] signals are ineffective, and appetite is not modified', said researcher Professor Baoji Xu from the Georgetown Medical Centre in the USA.
When the team monitored the eating habits of mice with and without the mutation, they found males were twice as heavy as their normal counterparts, and females were 2.7 times heavier. This was to do with them over-eating, rather than a reduction in their activity levels...
New neurons, a recipe for obesity?
An elusive metabolic 'switch' that significantly decreases weight-gain and increases energy consumption in mice, even when fed a high-fat diet, has been uncovered.
If a similar mechanism is found in humans, these findings, published in Nature Neuroscience today, may present a new target for potential treatments aimed at combating diet-induced weight gain and obesity.
"We've identified a region within the mouse hypothalamus in which new neurons are generated in both the postnatal and adult period. Neurogenesis in this area is stimulated by a high-fat diet, and blocking neurogenesis in this region attenuated weight gain on high fat diet," said lead author Seth Blackshaw from the Solomon H. Snyder Department of Neuroscience at Johns Hopkins University in the U.S...
If a similar mechanism is found in humans, these findings, published in Nature Neuroscience today, may present a new target for potential treatments aimed at combating diet-induced weight gain and obesity.
"We've identified a region within the mouse hypothalamus in which new neurons are generated in both the postnatal and adult period. Neurogenesis in this area is stimulated by a high-fat diet, and blocking neurogenesis in this region attenuated weight gain on high fat diet," said lead author Seth Blackshaw from the Solomon H. Snyder Department of Neuroscience at Johns Hopkins University in the U.S...
Fat gene linked to diabetes battle
A fat gene has been identified that appears to protect against diabetes.
The discovery suggests that, contrary to popular belief, fatty adipose tissue can benefit the body's metabolism.
Research shows how the gene, ChREBP, resists diabetes by converting glucose sugar into fatty acids. It also boosts sensitivity to insulin, the vital hormone that regulates blood sugar.
However, in most obese people, sugar is blocked from entering fat cells and blood sugar levels rise.
Eventually, this leads to insulin resistance and type-2 diabetes.
Scientists believe the findings could lead to new treatments for diabetes and other metabolic diseases.
They add to previous research based on 123 fat samples from non-diabetic people which showed the gene was more active in those whose bodies had a better sugar balance.
The fat gene's activity also correlated with insulin sensitivity in obese, non-diabetic people.
'The general concept of fat as all bad is not true,' said lead investigator Dr Mark Herman from Harvard Medical School in the US.
'Obesity is commonly associated with metabolic dysfunction that puts people at higher risk for diabetes, stroke and heart disease but there is a large percentage of obese people who are metabolically healthy.
'We started with a mouse model that disassociates obesity from its adverse effects.'...
The discovery suggests that, contrary to popular belief, fatty adipose tissue can benefit the body's metabolism.
Research shows how the gene, ChREBP, resists diabetes by converting glucose sugar into fatty acids. It also boosts sensitivity to insulin, the vital hormone that regulates blood sugar.
However, in most obese people, sugar is blocked from entering fat cells and blood sugar levels rise.
Eventually, this leads to insulin resistance and type-2 diabetes.
Scientists believe the findings could lead to new treatments for diabetes and other metabolic diseases.
They add to previous research based on 123 fat samples from non-diabetic people which showed the gene was more active in those whose bodies had a better sugar balance.
The fat gene's activity also correlated with insulin sensitivity in obese, non-diabetic people.
'The general concept of fat as all bad is not true,' said lead investigator Dr Mark Herman from Harvard Medical School in the US.
'Obesity is commonly associated with metabolic dysfunction that puts people at higher risk for diabetes, stroke and heart disease but there is a large percentage of obese people who are metabolically healthy.
'We started with a mouse model that disassociates obesity from its adverse effects.'...
Beer may improve health of obese people?
Hops compounds improve health of obese diabetic mice
A class of compounds found in hops, the crop generally known for its role in beer production, reduces weight gain in obese and diabetic mice, according to a study published Mar. 28 in the open access journal PLoS ONE. Eight weeks of treatment with the compounds, called tetrahydro iso-alpha acids, also reduced gut permeability and normalized insulin sensitivity markers in the mice, among other beneficial metabolic effects.
Hops have been known to contain anti-inflammatory compounds with potential medicinal uses for metabolic disorders, like insulin resistance and type 2 diabetes, which are associated with low-grade inflammation. These new results suggest a novel mechanism contributing to the positive effects of the investigated treatment, the authors write. The work was led by Patrice Cani of the Université catholique de Louvain in Brussels, Belgium.
A class of compounds found in hops, the crop generally known for its role in beer production, reduces weight gain in obese and diabetic mice, according to a study published Mar. 28 in the open access journal PLoS ONE. Eight weeks of treatment with the compounds, called tetrahydro iso-alpha acids, also reduced gut permeability and normalized insulin sensitivity markers in the mice, among other beneficial metabolic effects.
Hops have been known to contain anti-inflammatory compounds with potential medicinal uses for metabolic disorders, like insulin resistance and type 2 diabetes, which are associated with low-grade inflammation. These new results suggest a novel mechanism contributing to the positive effects of the investigated treatment, the authors write. The work was led by Patrice Cani of the Université catholique de Louvain in Brussels, Belgium.
Are antibiotics making you fat?
Listen to any TV commercial for a new drug and you'll hear a litany of bizarre side effects — amnesia, hallucinations, nightmares, blue urine and a furry-feeling tongue, just to name a few. But few of these lists include obesity, and overdosing on antibiotics, according to an article published in the magazine New Scientist, could be a major trigger for obesity.
People who overuse antibiotics have lower levels of good bacteria in their guts, and those good bacteria have been found to help prevent everything from cancer to obesity. A number of studies on mice have found that mice fed antibiotics at levels comparable to those given to farm animals are much heavier than mice fed no antibiotics at all — which isn't surprising, considering that antibiotics are often used to speed growth and fatten up animals for slaughter.
But what is concerning are the studies of antibiotics fed to mice at levels similar to what children receive when they get infections. In one study, microbiologist Martin Blaser, of New York University, fed mice short courses of antibiotics similar to those that children receive. Compared to the non-drugged mice, the antibiotic-fed mice had lower levels of T-cells, which regulate the body's immune response. Obesity has been associated with low levels of these T-cells...
People who overuse antibiotics have lower levels of good bacteria in their guts, and those good bacteria have been found to help prevent everything from cancer to obesity. A number of studies on mice have found that mice fed antibiotics at levels comparable to those given to farm animals are much heavier than mice fed no antibiotics at all — which isn't surprising, considering that antibiotics are often used to speed growth and fatten up animals for slaughter.
But what is concerning are the studies of antibiotics fed to mice at levels similar to what children receive when they get infections. In one study, microbiologist Martin Blaser, of New York University, fed mice short courses of antibiotics similar to those that children receive. Compared to the non-drugged mice, the antibiotic-fed mice had lower levels of T-cells, which regulate the body's immune response. Obesity has been associated with low levels of these T-cells...
Compounds Created That Dramatically Alter Biological Clock And Lead To Weight Loss, Metabolic Changes
Scientists from the Florida campus of The Scripps Research Institute have synthesized a pair of small molecules that dramatically alter the core biological clock in animal models, highlighting the compounds' potential effectiveness in treating a remarkable range of disorders-including obesity, diabetes, high cholesterol, and serious sleep disorders.
The study was published on March 29, 2012, in an advance, online edition of the journal Nature.
The study showed that when administered in animal models the synthetic small molecules altered circadian rhythm and the pattern of core clock gene expression in the brain's hypothalamus, the site of the master cellular clock that synchronizes daily rhythms in mammals; circadian rhythms are the physiological processes that respond to a 24-hour cycle of light and dark and are present in most living things.
When given to diet-induced obese mice, these same small molecules decreased obesity by reducing fat mass and markedly improving cholesterol levels and hyperglycemia - chronically high blood sugar levels that frequently lead to diabetes...
The study was published on March 29, 2012, in an advance, online edition of the journal Nature.
The study showed that when administered in animal models the synthetic small molecules altered circadian rhythm and the pattern of core clock gene expression in the brain's hypothalamus, the site of the master cellular clock that synchronizes daily rhythms in mammals; circadian rhythms are the physiological processes that respond to a 24-hour cycle of light and dark and are present in most living things.
When given to diet-induced obese mice, these same small molecules decreased obesity by reducing fat mass and markedly improving cholesterol levels and hyperglycemia - chronically high blood sugar levels that frequently lead to diabetes...
Wednesday, March 14, 2012
Cannabis chemical keeps mice slim
A natural cannabis-like chemical in the brain may hold the key to keeping couch potatoes slim, early research suggests.
Scientists in the US found that blocking the compound allowed mice to gorge on high fat food and take little exercise without putting on weight or becoming unhealthy.
The genetically modified animals produced limited amounts of the endocannabinoid 2-AG, a chemical related to the active ingredient in cannabis.
All mammalian brains, including those of humans, contain 2-AG, which is believed to control neural circuits involved in metabolism.
"We discovered that these mice were resistant to obesity because they burned fat calories much more efficiently than normal mice do," said study leader Professor Daniele Piomelli, from the University of California at Irvine.
"We had known that endocannabinoids play a critical role in cell energy regulation, but this is the first time we found a target where this occurs."
The mice stayed slim because they developed a hyperactive form of "brown fat" - a special type of fat that generates heat and keeps animals warm.
Not only did they not gain weight when fed a high-fat diet, but they failed to develop any of the expected signs of metabolic syndrome. This is a combination of problems such as obesity and high blood pressure which increase the risk of heart disease and diabetes...
Scientists in the US found that blocking the compound allowed mice to gorge on high fat food and take little exercise without putting on weight or becoming unhealthy.
The genetically modified animals produced limited amounts of the endocannabinoid 2-AG, a chemical related to the active ingredient in cannabis.
All mammalian brains, including those of humans, contain 2-AG, which is believed to control neural circuits involved in metabolism.
"We discovered that these mice were resistant to obesity because they burned fat calories much more efficiently than normal mice do," said study leader Professor Daniele Piomelli, from the University of California at Irvine.
"We had known that endocannabinoids play a critical role in cell energy regulation, but this is the first time we found a target where this occurs."
The mice stayed slim because they developed a hyperactive form of "brown fat" - a special type of fat that generates heat and keeps animals warm.
Not only did they not gain weight when fed a high-fat diet, but they failed to develop any of the expected signs of metabolic syndrome. This is a combination of problems such as obesity and high blood pressure which increase the risk of heart disease and diabetes...
The genetic tweak that 'could help us stay cancer free and remain thin no matter how much we eat'
Scientists have made a potential breakthrough against both cancer and obesity after identifying a way of modifying a gene that controls cell growth.
Mice given an extra copy of the anti-cancer gene Pten were less prone to weight gain and were more resistant to the disease.
The Pten gene is key in controlling cell growth in both mice and humans.
The study by the Spanish National Cancer Research Center also found that the creatures with adapted genes lived longer...
Mice given an extra copy of the anti-cancer gene Pten were less prone to weight gain and were more resistant to the disease.
The Pten gene is key in controlling cell growth in both mice and humans.
The study by the Spanish National Cancer Research Center also found that the creatures with adapted genes lived longer...
Fighting obesity without exercise or healthy diet possible? (Research)
Tired of trying everything but still not losing that weight? Here’s new research which might help you.
Blocking a brain compound may have a magical effect in burning fat, even if you gorge yourself and avoid the gym, a study reveals. For instance, mice modified to limit production of the brain compound, an endocannabinoid called 2-AG, did not gain any weight, even after being fed high fat diets and becoming sluggish. Neither did they develop any signs of obesity and high blood pressure linked ith cardiovascular disease and diabetes, the journal Cell Metabolism reported...
Blocking a brain compound may have a magical effect in burning fat, even if you gorge yourself and avoid the gym, a study reveals. For instance, mice modified to limit production of the brain compound, an endocannabinoid called 2-AG, did not gain any weight, even after being fed high fat diets and becoming sluggish. Neither did they develop any signs of obesity and high blood pressure linked ith cardiovascular disease and diabetes, the journal Cell Metabolism reported...
Genetic Tweak Helps Mice Avoid Cancer, Obesity: Study
New research offers potential insight into the connection between cancer, obesity and longevity in humans by showing that genetically modified mice live longer, skinnier and almost cancer-free lives.
There are quite a few differences between mice and humans, especially in regard to the type of fat that's apparently affected by the genetic tweak, so there's no way to know if the research could lead to benefits in humans. Even if medications based on the research are developed, no one knows what the side effects in people might be or their eventual cost...
There are quite a few differences between mice and humans, especially in regard to the type of fat that's apparently affected by the genetic tweak, so there's no way to know if the research could lead to benefits in humans. Even if medications based on the research are developed, no one knows what the side effects in people might be or their eventual cost...
Sunday, March 04, 2012
Heart Hormone Linked to Calorie-Burning Brown Fat
You may have heard about brown fat -- a unique type of fat that acts like a furnace in the body to burn calories instead of storing them as excess weight.
Adults don’t have much brown fat, but a new study suggests that hormones produced by the heart just might help them make more.
Researchers found that the hormones, known as cardiac natriuretic peptides, caused regular energy-storing white fat cells to turn into energy-burning brown fat in mice.
If studies show the same thing in humans, the heart hormone may hold the key to an effective weight loss treatment, says researcher Sheila Collins, PhD, of Sanford-Burnham Medical Research Institute in Orlando, Fla.
The study appears online in the Journal of Clinical Investigation.
“These hormones are involved in fluid regulation, but we showed in this study that they also play a role in breaking down fat,” she says.
Brown Fat and Heart Hormones
Collins and colleagues have long studied how the body’s adrenaline system regulates fat storage and weight loss.
In their latest work, they showed that the heart-derived hormones activate the same fat-burning process as the adrenaline pathway and that the two systems can work together to promote the browning of fat cells.
When they exposed mice to cold, the mice exhibited elevated amounts of natriuretic peptides in their circulatory systems, which turned on the fat-burning brown fat...
Adults don’t have much brown fat, but a new study suggests that hormones produced by the heart just might help them make more.
Researchers found that the hormones, known as cardiac natriuretic peptides, caused regular energy-storing white fat cells to turn into energy-burning brown fat in mice.
If studies show the same thing in humans, the heart hormone may hold the key to an effective weight loss treatment, says researcher Sheila Collins, PhD, of Sanford-Burnham Medical Research Institute in Orlando, Fla.
The study appears online in the Journal of Clinical Investigation.
“These hormones are involved in fluid regulation, but we showed in this study that they also play a role in breaking down fat,” she says.
Brown Fat and Heart Hormones
Collins and colleagues have long studied how the body’s adrenaline system regulates fat storage and weight loss.
In their latest work, they showed that the heart-derived hormones activate the same fat-burning process as the adrenaline pathway and that the two systems can work together to promote the browning of fat cells.
When they exposed mice to cold, the mice exhibited elevated amounts of natriuretic peptides in their circulatory systems, which turned on the fat-burning brown fat...
‘Epigenetics’ May Help Obese Persons; Other Uses Include Treatment of Aging, Inherited Diseases and Cancer
A new study at Sydney's Victor Chang Cardiac Research Institute showed that traits can be changed through "epigenetic" changes, which could have implications for a number of trends and changes in our population, such as the obesity epidemic.
Epigenetics is the study of heritable changes in gene expression or cellular phenotype caused by mechanisms other than changes in the underlying DNA sequence. It considers how genes are switched on or off, usually through an environmental stimulus, such as a change in diet.
However, unlike the genetic changes, epigenetic changes do not involve permanent mutations in the genetic code.
In their study, the researchers fed a group of mice a diet rich in supplements such as folate, zinc and vitamin B12, which help to suppress obesity in mice by turning a particular gene off.
The researchers found that when the diet was continued in the lean mice over five generations, the epigenetic effects were inherited which resulted in the increase in the proportion of lean and healthy specimens in each subsequent generation, without any change to the genetic code of the mice...
Epigenetics is the study of heritable changes in gene expression or cellular phenotype caused by mechanisms other than changes in the underlying DNA sequence. It considers how genes are switched on or off, usually through an environmental stimulus, such as a change in diet.
However, unlike the genetic changes, epigenetic changes do not involve permanent mutations in the genetic code.
In their study, the researchers fed a group of mice a diet rich in supplements such as folate, zinc and vitamin B12, which help to suppress obesity in mice by turning a particular gene off.
The researchers found that when the diet was continued in the lean mice over five generations, the epigenetic effects were inherited which resulted in the increase in the proportion of lean and healthy specimens in each subsequent generation, without any change to the genetic code of the mice...
The role of the brain in obesity
Researchers from the French Inserm institute have tested young mice with a diet rich in sugar and fat… And guess what? This diet completely modified their enteric nervous system (ENS).
In addition to our “principal” brain, protected by the skull, our organism is helped by a “second” brain: a group of nearly 100 million neurons lodged in the digestive tube – the enteric nervous system (ENS). And its main job? To regulate digestive function, such as gastric drainage, colonic transit, absorption of nutrients and the regulation of food intake...
In addition to our “principal” brain, protected by the skull, our organism is helped by a “second” brain: a group of nearly 100 million neurons lodged in the digestive tube – the enteric nervous system (ENS). And its main job? To regulate digestive function, such as gastric drainage, colonic transit, absorption of nutrients and the regulation of food intake...
Obesity could be INFECTIOUS: Gut microbe imbalance is catching, study finds
We all know of couples who piled on the pounds once they married and fat friends who seem to encourage each others bad eating habits.
But scientists have now claimed that chubbiness could be catching.
A study from Yale University found that both obesity and liver disease can be triggered by a family of proteins called inflammasomes that alter the balance of microbes in the stomach.
Amazingly, this altered intestinal environment can be passed on - making obesity an infectious condition.
The finding came to light during a study on stomach bacteria in mice...
But scientists have now claimed that chubbiness could be catching.
A study from Yale University found that both obesity and liver disease can be triggered by a family of proteins called inflammasomes that alter the balance of microbes in the stomach.
Amazingly, this altered intestinal environment can be passed on - making obesity an infectious condition.
The finding came to light during a study on stomach bacteria in mice...
Mutation of fat-related gene raises risk of obesity: study
A team of researchers from Kyoto University and a French national laboratory have become the world's first to discover that a mutation in a gene related to the detection of fats that enter the body raises the risk of obesity when fatty meals are eaten, according to the online version of the journal Nature posted Monday.
The gene, called GPR120, can also cause fatty liver if it mutates, because in such a case, the organ's ability to burn fat diminishes.
"Diagnosing the gene could help prevent symptoms resulting from metabolic syndrome and their treatment," said Gozo Tsujimoto, a Kyoto University professor and member of the team.
The international team gave fatty feed to two groups of mice -- one in which the GPR120 gene was deactivated and the other in which it was left active. The team found the mice in the group with the deactivated gene gained 15 percent more weight than the other group, while the total amount of body fat turned out to be double the amount in the mice with the normal gene.
The research also showed that the mice with deactivated GPR120 gene exhibited symptoms of fatty liver and diabetes...
The gene, called GPR120, can also cause fatty liver if it mutates, because in such a case, the organ's ability to burn fat diminishes.
"Diagnosing the gene could help prevent symptoms resulting from metabolic syndrome and their treatment," said Gozo Tsujimoto, a Kyoto University professor and member of the team.
The international team gave fatty feed to two groups of mice -- one in which the GPR120 gene was deactivated and the other in which it was left active. The team found the mice in the group with the deactivated gene gained 15 percent more weight than the other group, while the total amount of body fat turned out to be double the amount in the mice with the normal gene.
The research also showed that the mice with deactivated GPR120 gene exhibited symptoms of fatty liver and diabetes...
Animal study finds surprising clues to obesity-induced infertility
Infertility is common among obese women, but the reasons remain poorly understood and few treatments exist. Now a team of Johns Hopkins Children’s Center scientists, conducting experiments in mice, has uncovered what it considers surprising evidence that insulin resistance, long considered a prime suspect, has little to do with infertility in women with type 2 diabetes, polycystic ovary syndrome or metabolic syndrome, all obesity-related conditions in which the body becomes desensitized to insulin and loses the ability to regulate blood sugar.
In a report published online Nov.10 in the journal Diabetes, the Johns Hopkins scientists say that the real culprit appears to be insulin sensitivity in the ovaries and the pituitary.
The Johns Hopkins team said that its findings show that these organs escape insulin resistance and, awash with high levels of circulating insulin common in obesity, develop abnormal cell signaling that disrupts ovulation and eventually leads to infertility.
“Our findings suggest that the focus should shift from treating insulin resistance in peripheral tissue to taming insulin sensitivity in the pituitary and ovaries,” said lead investigator Sheng Wu, of the Johns Hopkins Children’s Center. Scientists traditionally have treated obesity-induced infertility by lowering blood insulin to counter the effects of insulin resistance...
In a report published online Nov.10 in the journal Diabetes, the Johns Hopkins scientists say that the real culprit appears to be insulin sensitivity in the ovaries and the pituitary.
The Johns Hopkins team said that its findings show that these organs escape insulin resistance and, awash with high levels of circulating insulin common in obesity, develop abnormal cell signaling that disrupts ovulation and eventually leads to infertility.
“Our findings suggest that the focus should shift from treating insulin resistance in peripheral tissue to taming insulin sensitivity in the pituitary and ovaries,” said lead investigator Sheng Wu, of the Johns Hopkins Children’s Center. Scientists traditionally have treated obesity-induced infertility by lowering blood insulin to counter the effects of insulin resistance...
Monday, February 20, 2012
Lipid Sensor GPR120 Linked to Obesity in Mice and Humans
A protein that acts as a lipid sensor, GPR120, can lead to obesity when defective in mice and humans, according to a study published online Feb. 19 in Nature...
Sunday, February 12, 2012
Four Natural Extracts With Anti-Obesity Effects Tested On Rats
University of Granada researchers have identified four plant extracts that might help in preventing and fighting obesity. The researchers identified the most effective plant extracts through in vitro assays; subsequently, extracts were tested on rats. While the results obtained are promising, further studies on animals are required to evaluate and confirm the anti-obesity effects of these extracts. Once their anti-obesity effects are confirmed on animals, the extracts will be tested on humans...
Saturday, February 11, 2012
NIH grant targets inflammation in link between obesity and disease
Preliminary results in mice point way to a potential treatment
If you are obese, you are at great risk of developing heart disease and diabetes. But research now underway at Eastern Virginia Medical School could drastically improve your odds of avoiding these serious diseases.
EVMS has secured a major, five-year research grant from the National Institutes of Health that may lead to ways to prevent the development of these diseases linked to obesity. The $1.8 million grant supports a multidisciplinary study of how to safely thwart chronic inflammation; scientists believe that inflammation triggers disease in people who are overweight.
"Inflammation is key to why central 'belly' fat leads to high risks for diabetes, heart disease and maybe even some forms of cancer," says Jerry L. Nadler, MD, director of the EVMS Strelitz Diabetes Center and principal investigator on the grant.
Inflammation is vital to our health. The immune system uses acute inflammation to battle certain infections and heal wounds; it subsides when no longer needed. But chronic inflammation can cause problems. It is this long-term inflammation that Dr. Nadler and his colleagues are targeting.
Obesity — now at epidemic levels in the United Sates — represents a major public-health challenge for the nation. The risk of having a heart attack triples during obesity. Nearly 80 percent of people who develop type 2 diabetes (often as a result of obesity) also develop heart disease...
If you are obese, you are at great risk of developing heart disease and diabetes. But research now underway at Eastern Virginia Medical School could drastically improve your odds of avoiding these serious diseases.
EVMS has secured a major, five-year research grant from the National Institutes of Health that may lead to ways to prevent the development of these diseases linked to obesity. The $1.8 million grant supports a multidisciplinary study of how to safely thwart chronic inflammation; scientists believe that inflammation triggers disease in people who are overweight.
"Inflammation is key to why central 'belly' fat leads to high risks for diabetes, heart disease and maybe even some forms of cancer," says Jerry L. Nadler, MD, director of the EVMS Strelitz Diabetes Center and principal investigator on the grant.
Inflammation is vital to our health. The immune system uses acute inflammation to battle certain infections and heal wounds; it subsides when no longer needed. But chronic inflammation can cause problems. It is this long-term inflammation that Dr. Nadler and his colleagues are targeting.
Obesity — now at epidemic levels in the United Sates — represents a major public-health challenge for the nation. The risk of having a heart attack triples during obesity. Nearly 80 percent of people who develop type 2 diabetes (often as a result of obesity) also develop heart disease...
Study Unlocks Secrets of Red Wine Chemical
If you love to sit back and sip a glass of cabernet or pinot noir, you can feel good knowing that the health benefits of red wine are now a little less mysterious. Scientists have uncovered how resveratrol, the chemical found in grape skins, peanuts and dark chocolate, works in mice to help fight several chronic diseases.
For the past decade, researchers have been intrigued by the apparent health benefits of resveratrol, which has been shown to fight obesity, type 2 diabetes and cancer in mice and seems to have some health benefits for humans. But no one understood how the chemical worked its magic on the body.
Now a new study from the National Institutes of Health has deciphered just how the chemical interacts with the body’s cells. The research is complicated, but spells out good news for the potential of the red-wine compound to treat chronic diseases.
Dr. Jay Chung, the study’s lead author, said resveratrol is tricky because it’s a “dirty molecule,” meaning it interacts in lots of different ways with the cells of the body, some good and some bad. By first testing cells in the lab and then testing mice, Chung and his team were able to identify which of resveratrol’s cellular hook-ups delivered the chemical’s benefits...
For the past decade, researchers have been intrigued by the apparent health benefits of resveratrol, which has been shown to fight obesity, type 2 diabetes and cancer in mice and seems to have some health benefits for humans. But no one understood how the chemical worked its magic on the body.
Now a new study from the National Institutes of Health has deciphered just how the chemical interacts with the body’s cells. The research is complicated, but spells out good news for the potential of the red-wine compound to treat chronic diseases.
Dr. Jay Chung, the study’s lead author, said resveratrol is tricky because it’s a “dirty molecule,” meaning it interacts in lots of different ways with the cells of the body, some good and some bad. By first testing cells in the lab and then testing mice, Chung and his team were able to identify which of resveratrol’s cellular hook-ups delivered the chemical’s benefits...
Researchers find obesity begins in brain
Though most people think obesity is a problem of hips, thighs and bellies, a new study by US scientists shows that obesity begins in the brain where the female hormone estrogen plays a role.
The study by a group of researchers, led by Baylor College of Medicine and The University of Texas Southwestern Medical School, shows that the hormone works through two populations of neurons, steroidogenic factor-1 (SF-1) neurons and the pro-opiomelanocortin (POMC) neurons, in a particular part of the brain called the hypothalamus.
The researchers found that the two kinds of neurons play different but important roles in metabolism, fat distribution and appetite control, according to the February issue of the Baylor College of Medicine news.
"Before menopause, women are protected from obesity and associated disorders by estrogen," said Dr. Yong Xu, the first author of the study and assistant professor of the USDA Agricultural Research Service Children's Nutrition Research Center at BCM and Texas Children's Hospital.
After menopause, the risk of obesity in women rises, while the risks of estrogen replacement therapy outweigh its effect on reducing obesity, Xu said.
Researchers studied four different kinds of mice to determine the effect of estrogen and focused their work on neurons in the hypothalamus that carry an estrogen receptor alpha. The hypothalamus links the nervous system to the endocrine system to regulate multiple physiological processes, including those controlling bodyweight...
The study by a group of researchers, led by Baylor College of Medicine and The University of Texas Southwestern Medical School, shows that the hormone works through two populations of neurons, steroidogenic factor-1 (SF-1) neurons and the pro-opiomelanocortin (POMC) neurons, in a particular part of the brain called the hypothalamus.
The researchers found that the two kinds of neurons play different but important roles in metabolism, fat distribution and appetite control, according to the February issue of the Baylor College of Medicine news.
"Before menopause, women are protected from obesity and associated disorders by estrogen," said Dr. Yong Xu, the first author of the study and assistant professor of the USDA Agricultural Research Service Children's Nutrition Research Center at BCM and Texas Children's Hospital.
After menopause, the risk of obesity in women rises, while the risks of estrogen replacement therapy outweigh its effect on reducing obesity, Xu said.
Researchers studied four different kinds of mice to determine the effect of estrogen and focused their work on neurons in the hypothalamus that carry an estrogen receptor alpha. The hypothalamus links the nervous system to the endocrine system to regulate multiple physiological processes, including those controlling bodyweight...
Can we ‘catch’ obesity and liver disease? Mice can
Here’s a new study from Yale University that adds another layer of complexity to the obesity puzzle: Lab mice whose intestinal enviroments were altered to create a deficiency in their immune responses developed a population of microbes in their stomachs that led to obesity and liver disease.
And healthy mice, when put in cages with the infected mice, developed the same population of microbes and the same propensity for obesity, metabolic syndrome and chronic liver disease...
And healthy mice, when put in cages with the infected mice, developed the same population of microbes and the same propensity for obesity, metabolic syndrome and chronic liver disease...
Exercise hormone can fight obesity
Irisin, a polypeptide hormone found in both humans and mice is a membrane protein in muscle cells that breaks down during exercise and secreted as a hormone, said researchers at the Dana-Farber Cancer Institute and Harvard Medical School in the US.
The hormone which is named after Iris, the messenger of the gods in Greek mythology acts as a chemical messenger and induces ordinary “white” fat cells to convert into “brown fat,” a type of adipose tissue that helps regulate body temperature, while burning a tremendous amount of energy in the process.
After injecting irisin into mice, researchers found that the hormone switched on genes that convert white fat into “good” brown fat which burns off more excess calories than does exercise alone, says the report published in the journal Nature...
The hormone which is named after Iris, the messenger of the gods in Greek mythology acts as a chemical messenger and induces ordinary “white” fat cells to convert into “brown fat,” a type of adipose tissue that helps regulate body temperature, while burning a tremendous amount of energy in the process.
After injecting irisin into mice, researchers found that the hormone switched on genes that convert white fat into “good” brown fat which burns off more excess calories than does exercise alone, says the report published in the journal Nature...
Could a pill help fight obesity?
Boston researchers have discovered a hormone produced by muscles during exercise which boosts the amount of calories the body burns.
In experiments with mice, Harvard Medical School researchers found that inducing greater levels of the hormone in obese, pre-diabetic mice led to weight loss, increased energy expenditure, and improvements in insulin resistance, which is a risk factor for diabetes...
In experiments with mice, Harvard Medical School researchers found that inducing greater levels of the hormone in obese, pre-diabetic mice led to weight loss, increased energy expenditure, and improvements in insulin resistance, which is a risk factor for diabetes...
Sunday, January 08, 2012
Fatty diet damages brain - study
SCIENTISTS have found a high-fat diet damages a crucial region of the brain that controls body weight in rodents and believe a similar process may occur in obese humans.
Within 24 hours of being fed high-fat foods, rats and mice developed inflammation followed by scarring in the hypothalamus, a region that regulates body weight and food intake in humans and rodents. Animals fed the diet continuously for four weeks developed chronic inflammation and neuron loss.
Within 24 hours of being fed high-fat foods, rats and mice developed inflammation followed by scarring in the hypothalamus, a region that regulates body weight and food intake in humans and rodents. Animals fed the diet continuously for four weeks developed chronic inflammation and neuron loss.
Obesity Linked to Brain Damage
...The notion that brain damage might play a role in body weight is not a new one, according to Michael Schwartz of the Diabetes and Obesity Center at the University of Washington in Seattle.
Scientists have known for about five years that the hypothalamus of overweight animals - including humans - displays inflammation, a typical reaction to injury.
But researchers, led by Schwartz, wanted to determine the role hypothalamus injury plays in obesity, and they had several questions they wanted to answer:
“Is it simply a consequence of becoming obese or does it occur before the obesity occurs?" says Schwartz. "And what could be driving that response? What is causing the inflammatory response and could that have something to do with the obesity itself?”
Schwartz’s team put laboratory mice and rats on a high-fat diet to make them gain weight. When they looked for evidence of inflammation in their brains, they made a startling discovery...
Scientists have known for about five years that the hypothalamus of overweight animals - including humans - displays inflammation, a typical reaction to injury.
But researchers, led by Schwartz, wanted to determine the role hypothalamus injury plays in obesity, and they had several questions they wanted to answer:
“Is it simply a consequence of becoming obese or does it occur before the obesity occurs?" says Schwartz. "And what could be driving that response? What is causing the inflammatory response and could that have something to do with the obesity itself?”
Schwartz’s team put laboratory mice and rats on a high-fat diet to make them gain weight. When they looked for evidence of inflammation in their brains, they made a startling discovery...
Saturday, December 17, 2011
Human enzyme keeps mice slim
A high-fat diet may not always pack on the pounds, new research from the Warren Alpert Medical School suggests. By successfully preventing weight gain in mice, researchers have shed light on obesity prevention in humans. The study was released online last week and will be published in the January 2012 issue of Endocrinology, a science journal.
Even though the mice were on a high-fat diet, researchers were able to significantly reduce their weight gain by activating a human enzyme called IKKbeta in their fatty tissue. The enzyme normally triggers immune responses, such as inflammation, following increases in the number of human fat cells.
Researchers were curious to see what would happen if they reversed the order of events by activating the enzyme prior to weight gain.
They found that in addition to reduced weight gain, the mice with the activated enzyme also had faster metabolisms. In these mice, insulin was more effective at lowering blood sugar than it was in the mice that had not been treated.
The activated enzyme also inhibited resistance to insulin, another side effect of obesity.
The study has definite implications for helping people who suffer from conditions characterized by insulin resistance, such as Type 2 diabetes patients, said Haiyan Xu, assistant professor of medicine...
Even though the mice were on a high-fat diet, researchers were able to significantly reduce their weight gain by activating a human enzyme called IKKbeta in their fatty tissue. The enzyme normally triggers immune responses, such as inflammation, following increases in the number of human fat cells.
Researchers were curious to see what would happen if they reversed the order of events by activating the enzyme prior to weight gain.
They found that in addition to reduced weight gain, the mice with the activated enzyme also had faster metabolisms. In these mice, insulin was more effective at lowering blood sugar than it was in the mice that had not been treated.
The activated enzyme also inhibited resistance to insulin, another side effect of obesity.
The study has definite implications for helping people who suffer from conditions characterized by insulin resistance, such as Type 2 diabetes patients, said Haiyan Xu, assistant professor of medicine...
New Weight-Loss Drug Reduces Body Weight in Monkeys, Mice
Researchers at the University of Texas MD Anderson Cancer Center have developed a drug that assaults the blood supply of fat cells and led to weight loss in obese rhesus monkeys.
Renata Pasqualini, Ph.D., co-senior author of the study and professor in MD Anderson's David H. Koch Center for Applied Research for Genitourinary Cancers, along with Wadih Arap, M.D., co-senior author of the study and a professor in the Koch Center, and Kirstin Barnhart, D.V.M., Ph.D., veterinary clinical pathologist at MD Anderson's Keeling Center for Comparative Medicine and Research, have created a new weight-loss drug that could potentially reduce accumulated white fat in humans.
Currently, weight-loss drugs work to suppress the appetite or increase metabolism in order to combat obesity, but harmful side effects come with the use of such drugs.
Now, Pasqualini and Arap have designed a new drug called Adipotide, which attacks white adipose tissue. This tissue is an unhealthy kind of fat that accumulates around the abdomen and under the skin. Adipotide contains a homing agent that attaches to a protein on the surface of blood vessels that support the fat. A synthetic peptide then triggers cell death, and with a lack of blood supply, the fat cells are reabsorbed.
The drug was used in mice models and rhesus monkey models. Adipotide was able to decrease abdominal circumference, body mass index (BMI) and body fat.
According to the study, the obese mice lost about 30 percent of their body weight while on Adipotide. The rhesus monkeys in the study, which were "spontaneously" obese due to overeating and a lack of physical activity, had a 27 percent decrease in abdominal fat levels. The drug reduced the weight of rhesus monkeys by 11 percent in just one month...
Renata Pasqualini, Ph.D., co-senior author of the study and professor in MD Anderson's David H. Koch Center for Applied Research for Genitourinary Cancers, along with Wadih Arap, M.D., co-senior author of the study and a professor in the Koch Center, and Kirstin Barnhart, D.V.M., Ph.D., veterinary clinical pathologist at MD Anderson's Keeling Center for Comparative Medicine and Research, have created a new weight-loss drug that could potentially reduce accumulated white fat in humans.
Currently, weight-loss drugs work to suppress the appetite or increase metabolism in order to combat obesity, but harmful side effects come with the use of such drugs.
Now, Pasqualini and Arap have designed a new drug called Adipotide, which attacks white adipose tissue. This tissue is an unhealthy kind of fat that accumulates around the abdomen and under the skin. Adipotide contains a homing agent that attaches to a protein on the surface of blood vessels that support the fat. A synthetic peptide then triggers cell death, and with a lack of blood supply, the fat cells are reabsorbed.
The drug was used in mice models and rhesus monkey models. Adipotide was able to decrease abdominal circumference, body mass index (BMI) and body fat.
According to the study, the obese mice lost about 30 percent of their body weight while on Adipotide. The rhesus monkeys in the study, which were "spontaneously" obese due to overeating and a lack of physical activity, had a 27 percent decrease in abdominal fat levels. The drug reduced the weight of rhesus monkeys by 11 percent in just one month...
Scripps Research scientists uncover new role for gene in maintaining steady weight
Against the backdrop of the growing epidemic of obesity in the United States, scientists from the Florida campus of The Scripps Research Institute have made an important new discovery regarding a specific gene that plays an important role in keeping a steady balance between our food intake and energy expenditure. The study may help scientists better understand the keys to fighting obesity and related disorders such as diabetes. The study, which was published in the November 25, 2011 print edition of The Journal of Biological Chemistry, focused on the melanocortin-3 receptor (MC3R), which normally responds to signals of nutrient intake.
"What we discovered was quite a surprise," said Scripps Research Associate Professor Andrew Butler, who led the study. "We thought that the actions of the receptor expressed in the brain would be critical for metabolic homeostasis. However, what we found is that actions of the receptor expressed outside the brain appear to be equally important."
The existence of drug targets in areas outside of the central nervous system (the body's "periphery") might help in the effort to develop drugs that influence metabolism without major side effects, Butler said.
The findings were made possible by the team's development of a new transgenic animal model, where expression of the MC3R gene can be selectively "switched on" in different cell types.
In the study, the suppression of MC3R expression in the brain and peripheral tissues had a marked impact on metabolic homeostasis (equilibrium). Interestingly, mice expressing the MC3R gene in the brain only displayed an obese phenotype (physical appearance) similar to those where all types of expression was suppressed, indicating that actions of this receptor in the brain are not sufficient to protect against weight gain.
"What we discovered was quite a surprise," said Scripps Research Associate Professor Andrew Butler, who led the study. "We thought that the actions of the receptor expressed in the brain would be critical for metabolic homeostasis. However, what we found is that actions of the receptor expressed outside the brain appear to be equally important."
The existence of drug targets in areas outside of the central nervous system (the body's "periphery") might help in the effort to develop drugs that influence metabolism without major side effects, Butler said.
The findings were made possible by the team's development of a new transgenic animal model, where expression of the MC3R gene can be selectively "switched on" in different cell types.
In the study, the suppression of MC3R expression in the brain and peripheral tissues had a marked impact on metabolic homeostasis (equilibrium). Interestingly, mice expressing the MC3R gene in the brain only displayed an obese phenotype (physical appearance) similar to those where all types of expression was suppressed, indicating that actions of this receptor in the brain are not sufficient to protect against weight gain.
Neuron Transplant Reduces Obesity In Mice
Scientists at Harvard University have successfully transplanted neurons into the brains of obesity-prone mice to prevent them from getting fat. The researchers did not have human obesity in mind when conducting the experiment; rather, they used the neuron transplant as an example of a method to restore function to abnormal neural circuits. The results have highlighted the promise in cell therapies. For example, scientists could soon transplant stem cells or fetal cells to treat nervous system diseases.
Throughout the years, research on cell therapies has rarely found success. Experiments using stem cell therapy to treat spinal injuries as well as some trials involving fetal cell therapy for Parkinson’s disease have yielded no positive results. Only until recent years has it been proven that the human brain produces new neurons throughout the lifetime. Some evidence has shown that these new neurons are occasionally integrated into existing neural circuits and actually enhance brain function. This evidence led scientists to postulate that this could be done using transplanted cells as well.
Obesity prone mice were used to test a special fetal stem cell therapy. | Photo courtesy of Bigplankton via Wikimedia Commons
The Harvard University scientists extracted healthy neurons from mouse embryos (the hypothalamus to be exact) and transplanted those neurons into the same region of the brain in obesity prone mice. These mice lack the receptor for leptin, a hormone that regulates metabolism and body weight, and therefore they are prone to being diabetic and obese. The transplanted neurons were labeled with a green fluorescent protein to track them in the neural circuit. The results were quite promising, as the transplanted neurons were able to integrate efficiently into the existing neural circuit and develop into mature neurons that responded to leptin. At the end of the experiment, the treated mice weighed 30% less than mice that had not received a transplant. This suggested that the transplanted neurons actually fixed the damaged neural circuit.
Though the experiment was not directed towards treating human obesity, the success of the experiment gave scientists a light at the end of the tunnel in terms of cell therapies...
Throughout the years, research on cell therapies has rarely found success. Experiments using stem cell therapy to treat spinal injuries as well as some trials involving fetal cell therapy for Parkinson’s disease have yielded no positive results. Only until recent years has it been proven that the human brain produces new neurons throughout the lifetime. Some evidence has shown that these new neurons are occasionally integrated into existing neural circuits and actually enhance brain function. This evidence led scientists to postulate that this could be done using transplanted cells as well.
Obesity prone mice were used to test a special fetal stem cell therapy. | Photo courtesy of Bigplankton via Wikimedia Commons
The Harvard University scientists extracted healthy neurons from mouse embryos (the hypothalamus to be exact) and transplanted those neurons into the same region of the brain in obesity prone mice. These mice lack the receptor for leptin, a hormone that regulates metabolism and body weight, and therefore they are prone to being diabetic and obese. The transplanted neurons were labeled with a green fluorescent protein to track them in the neural circuit. The results were quite promising, as the transplanted neurons were able to integrate efficiently into the existing neural circuit and develop into mature neurons that responded to leptin. At the end of the experiment, the treated mice weighed 30% less than mice that had not received a transplant. This suggested that the transplanted neurons actually fixed the damaged neural circuit.
Though the experiment was not directed towards treating human obesity, the success of the experiment gave scientists a light at the end of the tunnel in terms of cell therapies...
Weight-Loss Enzyme Identified by Brown Researchers
While not the solution to holiday weight gain, a new study from Brown University researchers sheds promising new light on metabolism and weight loss.
Scientists report that they substantially curbed weight gain, improved metabolism, and improved the efficacy of insulin in mice by engineering them to express a specific human enzyme in their fat tissue. Although the obesity prevention came at the significant cost of widespread inflammation, the research offers new clues about the connections among obesity, insulin resistance and type 2 diabetes, and inflammation...
Scientists report that they substantially curbed weight gain, improved metabolism, and improved the efficacy of insulin in mice by engineering them to express a specific human enzyme in their fat tissue. Although the obesity prevention came at the significant cost of widespread inflammation, the research offers new clues about the connections among obesity, insulin resistance and type 2 diabetes, and inflammation...
Cilia control eating signal
The action of tiny hairlike appendages on cells can mean the difference between fat and thin. Now scientists have a better idea of how the little hairs, called primary cilia, control appetite.
Primary cilia — single, hairlike projections that all cells in vertebrates usually have — seem to sequester a protein that senses and responds to an appetite-stimulating hormone, Nicolas Berbari of the University of Alabama at Birmingham reported December 6 at the annual meeting of the American Society for Cell Biology. In people and mice that lack primary cilia, the appetite stimulant works overtime, leading to overeating and obesity, Berbari said.
These findings may lead to new ways to control appetite and prevent or reverse obesity.
And the study may help scientists better understand the process of eating, said Kirk Mykytyn, a cell biologist at Ohio State University in Columbus. “This work is important because it’s more thoroughly clarifying the molecular mechanism involved in obesity associated with the loss of cilia,” he said...
Primary cilia — single, hairlike projections that all cells in vertebrates usually have — seem to sequester a protein that senses and responds to an appetite-stimulating hormone, Nicolas Berbari of the University of Alabama at Birmingham reported December 6 at the annual meeting of the American Society for Cell Biology. In people and mice that lack primary cilia, the appetite stimulant works overtime, leading to overeating and obesity, Berbari said.
These findings may lead to new ways to control appetite and prevent or reverse obesity.
And the study may help scientists better understand the process of eating, said Kirk Mykytyn, a cell biologist at Ohio State University in Columbus. “This work is important because it’s more thoroughly clarifying the molecular mechanism involved in obesity associated with the loss of cilia,” he said...
Saturday, November 26, 2011
Neuron Transplants Can Repair Brain Circuits
A new study by Harvard University neuroscientist Jeffrey Macklis and colleagues suggests it is possible to transplant fetal neurons into a part of the mouse brain that does not normally generate new brain cells, and they will repair abnormal circuits. In this case, the researchers repaired a genetic defect that causes obesity, but that was not the goal of their work which was to establish proof of principle that transplanted neurons can integrate into existing faulty brain circuits and restore them...
Sunday, November 20, 2011
New Weight-Loss Drug Reduces Body Weight in Monkeys, Mice
The new drug, called Adipotide, attacks white adipose tissue under the skin and around the abdomen
Researchers at the University of Texas MD Anderson Cancer Center have developed a drug that assaults the blood supply of fat cells and led to weight loss in obese rhesus monkeys.
Renata Pasqualini, Ph.D., co-senior author of the study and professor in MD Anderson's David H. Koch Center for Applied Research for Genitourinary Cancers, along with Wadih Arap, M.D., co-senior author of the study and a professor in the Koch Center, and Kirstin Barnhart, D.V.M., Ph.D., veterinary clinical pathologist at MD Anderson's Keeling Center for Comparative Medicine and Research, have created a new weight-loss drug that could potentially reduce accumulated white fat in humans.
Currently, weight-loss drugs work to suppress the appetite or increase metabolism in order to combat obesity, but harmful side effects come with the use of such drugs.
Now, Pasqualini and Arap have designed a new drug called Adipotide, which attacks white adipose tissue. This tissue is an unhealthy kind of fat that accumulates around the abdomen and under the skin. Adipotide contains a homing agent that attaches to a protein on the surface of blood vessels that support the fat. A synthetic peptide then triggers cell death, and with a lack of blood supply, the fat cells are reabsorbed.
The drug was used in mice models and rhesus monkey models. Adipotide was able to decrease abdominal circumference, body mass index (BMI) and body fat...
Researchers at the University of Texas MD Anderson Cancer Center have developed a drug that assaults the blood supply of fat cells and led to weight loss in obese rhesus monkeys.
Renata Pasqualini, Ph.D., co-senior author of the study and professor in MD Anderson's David H. Koch Center for Applied Research for Genitourinary Cancers, along with Wadih Arap, M.D., co-senior author of the study and a professor in the Koch Center, and Kirstin Barnhart, D.V.M., Ph.D., veterinary clinical pathologist at MD Anderson's Keeling Center for Comparative Medicine and Research, have created a new weight-loss drug that could potentially reduce accumulated white fat in humans.
Currently, weight-loss drugs work to suppress the appetite or increase metabolism in order to combat obesity, but harmful side effects come with the use of such drugs.
Now, Pasqualini and Arap have designed a new drug called Adipotide, which attacks white adipose tissue. This tissue is an unhealthy kind of fat that accumulates around the abdomen and under the skin. Adipotide contains a homing agent that attaches to a protein on the surface of blood vessels that support the fat. A synthetic peptide then triggers cell death, and with a lack of blood supply, the fat cells are reabsorbed.
The drug was used in mice models and rhesus monkey models. Adipotide was able to decrease abdominal circumference, body mass index (BMI) and body fat...
A specific human enzyme may help tackle obesity and diabetes, if a new scientific report is to be believed.
In a new study, scientists have reported that they substantially curbed weight gain, improved metabolism, and improved the efficacy of insulin in mice by engineering them to express a specific human enzyme in their fat tissue.
Although the obesity prevention came at the significant cost of widespread inflammation, the research offers new clues about the connections among obesity, insulin resistance and type 2 diabetes, and inflammation.
"Turning on this molecule has a very dramatic impact on lipid metabolism," said Haiyan Xu, assistant professor of medicine (research) in the Warren Alpert Medical School of Brown University and a researcher at Rhode Island Hospital's Hallett Center for Diabetes and Endocrinology.
In the study, the researchers changed the sequence of events for transgenically engineered mice by inducing inflammation via the enzyme IKKbeta in their fatty tissue before they were obese. The result for metabolism was much more positive than for control mice who were left unaltered but were fed the same diets...
In a new study, scientists have reported that they substantially curbed weight gain, improved metabolism, and improved the efficacy of insulin in mice by engineering them to express a specific human enzyme in their fat tissue.
Although the obesity prevention came at the significant cost of widespread inflammation, the research offers new clues about the connections among obesity, insulin resistance and type 2 diabetes, and inflammation.
"Turning on this molecule has a very dramatic impact on lipid metabolism," said Haiyan Xu, assistant professor of medicine (research) in the Warren Alpert Medical School of Brown University and a researcher at Rhode Island Hospital's Hallett Center for Diabetes and Endocrinology.
In the study, the researchers changed the sequence of events for transgenically engineered mice by inducing inflammation via the enzyme IKKbeta in their fatty tissue before they were obese. The result for metabolism was much more positive than for control mice who were left unaltered but were fed the same diets...
Thursday, November 17, 2011
Metabolism Boosted By Enzyme, Weight Gain Prevented In Mice
Male and female mice engineered to express the inflammatory enzyme IKKbeta in their fat tissue ate more but gained less weight. They burned sugar and fat more effectively than mice who were left unaltered. The research may shed light on how obesity and inflammation affect insulin resistance and sensitivity.
In a new study, scientists report that they substantially curbed weight gain, improved metabolism, and improved the efficacy of insulin in mice by engineering them to express a specific human enzyme in their fat tissue. Although the obesity prevention came at the significant cost of widespread inflammation, the research offers new clues about the connections among obesity, insulin resistance and type 2 diabetes, and inflammation...
In a new study, scientists report that they substantially curbed weight gain, improved metabolism, and improved the efficacy of insulin in mice by engineering them to express a specific human enzyme in their fat tissue. Although the obesity prevention came at the significant cost of widespread inflammation, the research offers new clues about the connections among obesity, insulin resistance and type 2 diabetes, and inflammation...
Sunday, November 13, 2011
Research Report: Hormone fights fat with fat
There are two types of body fat: white fat that stores energy and brown fat (packed with blood vessels and mitrochondria) that burns white fat. Long thought to disappear after infancy, brown fat has been rediscovered in adults humans using new imaging technology.
Sanford-Burnham Medical Research Institute researchers now report the discovery of orexin; a hormone that activates calorie-burning brown fat in mice. Orexin deficiency is associated with obesity, suggesting that supplemental orexin could lead to a new class of fat-fighting drugs focused on peripheral fat-burning tissue rather than the brain’s appetite control center which is the aim of most current weight-loss agents...
Sanford-Burnham Medical Research Institute researchers now report the discovery of orexin; a hormone that activates calorie-burning brown fat in mice. Orexin deficiency is associated with obesity, suggesting that supplemental orexin could lead to a new class of fat-fighting drugs focused on peripheral fat-burning tissue rather than the brain’s appetite control center which is the aim of most current weight-loss agents...
Microbes may be key to good health
Consider this: The average person's body contains about 100 trillion cells, but only maybe one in 10 is human.
This isn't the latest Hollywood horror flick, or some secret genetic engineering experiment run amok.
This, it turns out, is nature's way: The human cells that form our skin, eyes, ears, brain and every other part of our bodies are far outnumbered by those from microbes, primarily bacteria but also viruses, fungi and a panoply of other microorganisms.
That thought might make a lot of people lunge for the hand sanitizer, at the least. But that predictable impulse may be exactly the wrong one. A growing body of evidence indicates that the microbial ecosystems that have long populated our guts, mouths, noses and every other nook and cranny play crucial roles in keeping us healthy.
Moreover, researchers are becoming more convinced that modern trends -- diet, antibiotics, obsession with cleanliness, Caesarean delivery of babies --- are disrupting this delicate balance, contributing to some of the most perplexing ailments, including asthma, allergies, obesity, diabetes, autoimmune diseases, cancer and perhaps even autism.
"In terms of potential for human health, I would place it with stem cells as one of the two most promising areas of research at the moment," said Rob Knight of the University of Colorado. "Everywhere we look, microbes seem to be involved."
Equipped with super-fast new DNA decoders, scientists are accelerating the exploration of this realm at a molecular level, yielding provocative insights into how these microbial stowaways may wield far greater powers than previously appreciated in, paradoxically, making us human.
"The field has exploded," said Jeffrey Gordon of Washington University, who pioneered the exploration of humanity's microbial inhabitants, known as the "microbiome" or "microbiota." "People have this sense of wonderment about looking at themselves as a compilation of microbial and human parts."
Some equate these microbial inhabitants to a newly recognized organ. Acquired beginning at birth, this mass of fellow travelers may help steer normal development, molding immune systems and calibrating fundamental metabolic functions such as energy storage and consumption. There are even tantalizing clues they may help shape brain development, influencing behavior.
"The 'human supraorganism' is one term coined to describe the human host and all the attendant microorganisms," said Lita Proctor, who leads the Human Microbiome Project at the National Institutes of Health, which is mapping this world. "There's been a real revolution in thinking about what that means."
Investigators are trying to identify which organisms may truly be beneficial "probiotics" that people could take to help their health. Others are finding substances that people might ingest to nurture the good bugs. Drugs may mimic the helpful compounds that these organisms produce.
Doctors have even begun microbiota "transplants" to treat a host of illnesses, including a sometimes-devastating gastrointestinal infection called C. difficile, digestive system ailments such as Crohn's disease, colitis and irritable bowel disorder, and even in a handful of cases obesity and other afflictions, such as multiple sclerosis.
Many advocates of the research urge caution, noting that most of the work so far has involved laboratory animals or small numbers of patients, many hypotheses remain far from proven and nothing has zero risk.
"We have to be very careful in how we state what we know at the present time versus what we think might be true at this point," said David Relman of Stanford University. "But it's probably fair to say that our indigenous communities are more diverse, more complex and more intimately and intricately involved in our biology than we thought."
Scientists have long known that many organisms evolved with humans and perform vital functions, digesting food, extracting crucial nutrients, fighting off disease-causing entities.
But as microbiologists have begun scrutinizing these colonies, it has become clearer that they create carefully calibrated enterprises, with unique combinations inhabiting individual crevices and identifiable nuances from person to person.
European scientists reported in April that people generally seem to have one of three basic combinations that may be as fundamentally important as, say, blood type.
The five-year, $175 million U.S. Human Microbiome Project is assembling an outline of a "healthy" microbiome by sampling the mouth, airway, skin, gut and urogenital tract of 300 healthy adults, as well as deciphering the genetic codes of 200 possibly key microbes.
Dozens of studies are also underway, including some that are repeatedly swabbing kids and adults, including twins, to gain insights into why one person gets tooth decay, asthma, ulcerative colitis or even cancer, and another doesn't.
One intriguing finding is that babies born through Caesarean sections apparently miss out on acquiring their mothers' microbiota.
"The birth canal is very heavily colonized by bacteria," said Maria Dominguez-Bello, a University of Puerto Rico biologist who has been studying microbiota around the world, including in isolated tribes in the Amazon. "We think that is not by chance."
The interaction between the microbiota and the immune system may also play a role in other diseases in adults, including those caused at least in part by chronic inflammation from hyperactive immune systems.
"Gut bacteria have figured out a way to network with our immune system so it doesn't attack them," said Sarkis Mazmanian of the California Institute of Technology.
The microbiota apparently sends signals that dampen the "inflammatory response," a crucial defense also believed to play a role in a variety of diseases, including many forms of cancer, the "metabolic syndrome" caused by obesity, diabetes and heart disease.
The theory is that one reason some people may be prone to these diseases is that they are missing certain microbes. One anti-inflammatory compound produced by a bacterium appears to cure the equivalent of colitis and multiple sclerosis in mice, both of which are caused by misfiring immune systems, Mazmanian found.
Similarly, studies indicate that gut dwellers secrete messengers to cells lining the digestive tract to modulate key hormones, such as leptin and ghrelin, which are players in regulating metabolism, hunger and a sense of fullness.
Obese people appear to have a distinctive mix of digestive bacteria that make them prone to weight gain. Thin mice get fatter when their microbiota is replaced with the microbes of obese animals.
"Our ancient microbiome is losing the equilibrium it used to have with the host -- us -- and that has profound physiological consequences," said Martin Blaser of the New York University School of Medicine, who published his concerns in an August paper in the journal Nature.
Intriguing clues are also emerging about how microbes may affect the brain. Manipulating gut microbiomes of mice influences their anxiety and activity, Swedish researchers reported in January in the Proceedings of the National Academy of Sciences...
This isn't the latest Hollywood horror flick, or some secret genetic engineering experiment run amok.
This, it turns out, is nature's way: The human cells that form our skin, eyes, ears, brain and every other part of our bodies are far outnumbered by those from microbes, primarily bacteria but also viruses, fungi and a panoply of other microorganisms.
That thought might make a lot of people lunge for the hand sanitizer, at the least. But that predictable impulse may be exactly the wrong one. A growing body of evidence indicates that the microbial ecosystems that have long populated our guts, mouths, noses and every other nook and cranny play crucial roles in keeping us healthy.
Moreover, researchers are becoming more convinced that modern trends -- diet, antibiotics, obsession with cleanliness, Caesarean delivery of babies --- are disrupting this delicate balance, contributing to some of the most perplexing ailments, including asthma, allergies, obesity, diabetes, autoimmune diseases, cancer and perhaps even autism.
"In terms of potential for human health, I would place it with stem cells as one of the two most promising areas of research at the moment," said Rob Knight of the University of Colorado. "Everywhere we look, microbes seem to be involved."
Equipped with super-fast new DNA decoders, scientists are accelerating the exploration of this realm at a molecular level, yielding provocative insights into how these microbial stowaways may wield far greater powers than previously appreciated in, paradoxically, making us human.
"The field has exploded," said Jeffrey Gordon of Washington University, who pioneered the exploration of humanity's microbial inhabitants, known as the "microbiome" or "microbiota." "People have this sense of wonderment about looking at themselves as a compilation of microbial and human parts."
Some equate these microbial inhabitants to a newly recognized organ. Acquired beginning at birth, this mass of fellow travelers may help steer normal development, molding immune systems and calibrating fundamental metabolic functions such as energy storage and consumption. There are even tantalizing clues they may help shape brain development, influencing behavior.
"The 'human supraorganism' is one term coined to describe the human host and all the attendant microorganisms," said Lita Proctor, who leads the Human Microbiome Project at the National Institutes of Health, which is mapping this world. "There's been a real revolution in thinking about what that means."
Investigators are trying to identify which organisms may truly be beneficial "probiotics" that people could take to help their health. Others are finding substances that people might ingest to nurture the good bugs. Drugs may mimic the helpful compounds that these organisms produce.
Doctors have even begun microbiota "transplants" to treat a host of illnesses, including a sometimes-devastating gastrointestinal infection called C. difficile, digestive system ailments such as Crohn's disease, colitis and irritable bowel disorder, and even in a handful of cases obesity and other afflictions, such as multiple sclerosis.
Many advocates of the research urge caution, noting that most of the work so far has involved laboratory animals or small numbers of patients, many hypotheses remain far from proven and nothing has zero risk.
"We have to be very careful in how we state what we know at the present time versus what we think might be true at this point," said David Relman of Stanford University. "But it's probably fair to say that our indigenous communities are more diverse, more complex and more intimately and intricately involved in our biology than we thought."
Scientists have long known that many organisms evolved with humans and perform vital functions, digesting food, extracting crucial nutrients, fighting off disease-causing entities.
But as microbiologists have begun scrutinizing these colonies, it has become clearer that they create carefully calibrated enterprises, with unique combinations inhabiting individual crevices and identifiable nuances from person to person.
European scientists reported in April that people generally seem to have one of three basic combinations that may be as fundamentally important as, say, blood type.
The five-year, $175 million U.S. Human Microbiome Project is assembling an outline of a "healthy" microbiome by sampling the mouth, airway, skin, gut and urogenital tract of 300 healthy adults, as well as deciphering the genetic codes of 200 possibly key microbes.
Dozens of studies are also underway, including some that are repeatedly swabbing kids and adults, including twins, to gain insights into why one person gets tooth decay, asthma, ulcerative colitis or even cancer, and another doesn't.
One intriguing finding is that babies born through Caesarean sections apparently miss out on acquiring their mothers' microbiota.
"The birth canal is very heavily colonized by bacteria," said Maria Dominguez-Bello, a University of Puerto Rico biologist who has been studying microbiota around the world, including in isolated tribes in the Amazon. "We think that is not by chance."
The interaction between the microbiota and the immune system may also play a role in other diseases in adults, including those caused at least in part by chronic inflammation from hyperactive immune systems.
"Gut bacteria have figured out a way to network with our immune system so it doesn't attack them," said Sarkis Mazmanian of the California Institute of Technology.
The microbiota apparently sends signals that dampen the "inflammatory response," a crucial defense also believed to play a role in a variety of diseases, including many forms of cancer, the "metabolic syndrome" caused by obesity, diabetes and heart disease.
The theory is that one reason some people may be prone to these diseases is that they are missing certain microbes. One anti-inflammatory compound produced by a bacterium appears to cure the equivalent of colitis and multiple sclerosis in mice, both of which are caused by misfiring immune systems, Mazmanian found.
Similarly, studies indicate that gut dwellers secrete messengers to cells lining the digestive tract to modulate key hormones, such as leptin and ghrelin, which are players in regulating metabolism, hunger and a sense of fullness.
Obese people appear to have a distinctive mix of digestive bacteria that make them prone to weight gain. Thin mice get fatter when their microbiota is replaced with the microbes of obese animals.
"Our ancient microbiome is losing the equilibrium it used to have with the host -- us -- and that has profound physiological consequences," said Martin Blaser of the New York University School of Medicine, who published his concerns in an August paper in the journal Nature.
Intriguing clues are also emerging about how microbes may affect the brain. Manipulating gut microbiomes of mice influences their anxiety and activity, Swedish researchers reported in January in the Proceedings of the National Academy of Sciences...
Researchers Discover New Gene that Encodes for Diabetes Resistance
esearchers at the University of Wisconsin-Madison have identified a gene that may be responsible for determining an individual's susceptibility to both Type 1 and Type 2 diabetes. The study, which lasted over a decade, identified a gene in obese mice that controls a protein called tomosyn-2 - a compound responsible for decreased insulin production in pancreatic beta cells.
When insulin production in the pancreas is reduced diabetes can follow. Insulin is released into the bloodstream where it allows cells to absorb sugar and use it for energy. Individuals with Type 1 diabetes are insulin-deficient while those with Type 2 diabetes are insulin-resistant. Both forms of the disease cause significant complications, especially if it goes unmanaged.
The newly-discovered gene was found to affect insulin production in obese mice by reducing the activity of the protein tomosyn-2. While the gene can be controlled in mice, researchers will need to conduct further studies to determine whether medications that target the protein can be developed for humans.
"It's too early for us to know how relevant this gene will be to human diabetes, but the concept of negative regulation is one of the most interesting things to come out of this study and that very likely applies to humans," says Alan Attie, head of the study and biochemistry professor at University of Wisconsin-Madison.
The research team specifically used obese mice because they need more insulin to normalize blood glucose levels, especially after a meal, and humans have similar insulin needs. Being overweight requires more insulin to simply keep blood sugar levels regulated...
When insulin production in the pancreas is reduced diabetes can follow. Insulin is released into the bloodstream where it allows cells to absorb sugar and use it for energy. Individuals with Type 1 diabetes are insulin-deficient while those with Type 2 diabetes are insulin-resistant. Both forms of the disease cause significant complications, especially if it goes unmanaged.
The newly-discovered gene was found to affect insulin production in obese mice by reducing the activity of the protein tomosyn-2. While the gene can be controlled in mice, researchers will need to conduct further studies to determine whether medications that target the protein can be developed for humans.
"It's too early for us to know how relevant this gene will be to human diabetes, but the concept of negative regulation is one of the most interesting things to come out of this study and that very likely applies to humans," says Alan Attie, head of the study and biochemistry professor at University of Wisconsin-Madison.
The research team specifically used obese mice because they need more insulin to normalize blood glucose levels, especially after a meal, and humans have similar insulin needs. Being overweight requires more insulin to simply keep blood sugar levels regulated...
Estrogen Works in Brain To Regulate Female Weight
Estrogen regulates energy output, appetite and body weight, and insufficient estrogen receptors in certain regions of the brain may lead to obesity, according to a recent mouse study at the University of Texas Southwestern Medical Center.
“Estrogen has a profound effect on metabolism,” said Dr. Deborah Clegg, associate professor of internal medicine and senior author of the study. “We hadn’t previously thought of sex hormones as being critical regulators of food intake and body weight.”
The research is the first to demonstrate that estrogen works through two hypothalamic neural centers in the brain to regulate hunger and energy expenditure, keeping female body weight in check.
Female mice without the estrogen receptor alpha – a molecule that sends estrogen signals to neurons – in those parts of the brain became obese and developed related diseases, such as diabetes and heart disease.
These results were not replicated in male mice, although scientists believe other unknown estrogen receptor sites in the brain play a similar role in regulating male metabolism as well.
Although estrogen receptors are located throughout the body, researchers pinpointed two specific populations of estrogen receptors that seem to regulate energy balance for female mice...
“Estrogen has a profound effect on metabolism,” said Dr. Deborah Clegg, associate professor of internal medicine and senior author of the study. “We hadn’t previously thought of sex hormones as being critical regulators of food intake and body weight.”
The research is the first to demonstrate that estrogen works through two hypothalamic neural centers in the brain to regulate hunger and energy expenditure, keeping female body weight in check.
Female mice without the estrogen receptor alpha – a molecule that sends estrogen signals to neurons – in those parts of the brain became obese and developed related diseases, such as diabetes and heart disease.
These results were not replicated in male mice, although scientists believe other unknown estrogen receptor sites in the brain play a similar role in regulating male metabolism as well.
Although estrogen receptors are located throughout the body, researchers pinpointed two specific populations of estrogen receptors that seem to regulate energy balance for female mice...
Omega-3 key in reducing diabetes and heart disease
Omega-3 can help to reduce the risk of diabetes and heart disease especially as people age, says Massey University nutrition professor Bernhard Breier, co-author of a new international study.
Professor Breier, who leads an international research team, says omega-3s are especially beneficial for health in ageing because they improve carbohydrate and fat metabolism.
His research found a diet high in omega-3 fatty acids helps to burn metabolic fuels (glucose and fat) better, and can regulate energy storage across different tissues. This is despite genetic factors that predispose some people to gain weight more easily, making them potentially more susceptible to conditions such as diabetes and heart disease.
“These findings are important because the ageing process is closely linked with a higher risk of developing metabolic syndrome – a clustering of risk factors for heart disease, diabetes and obesity,” says Professor Breier, Chair of Human Nutrition at the Institute of Food, Nutrition and Human Health at Albany.
He says omega-3 fatty acids have been found to stimulate the process known as the insulin signalling cascade, which improves how blood sugar is used in the body. Researchers from Germany, Australia and New Zealand carried out tests on mice, examining the effects of feeding omega-3 rich diets to two groups with distinct, genetically determined traits to model different body types and metabolic responses of humans. One group developed obesity more easily and the second was a leaner variety.
When scientists measured changes to the metabolic responses, results showed the omega-3 rich diet reduced cholesterol and improved insulin action and fat metabolism in both groups of mice. However, the obesity prone mice responded less well than the leaner variety, drawing attention to genetically determined pathways that contribute to obesity...
Professor Breier, who leads an international research team, says omega-3s are especially beneficial for health in ageing because they improve carbohydrate and fat metabolism.
His research found a diet high in omega-3 fatty acids helps to burn metabolic fuels (glucose and fat) better, and can regulate energy storage across different tissues. This is despite genetic factors that predispose some people to gain weight more easily, making them potentially more susceptible to conditions such as diabetes and heart disease.
“These findings are important because the ageing process is closely linked with a higher risk of developing metabolic syndrome – a clustering of risk factors for heart disease, diabetes and obesity,” says Professor Breier, Chair of Human Nutrition at the Institute of Food, Nutrition and Human Health at Albany.
He says omega-3 fatty acids have been found to stimulate the process known as the insulin signalling cascade, which improves how blood sugar is used in the body. Researchers from Germany, Australia and New Zealand carried out tests on mice, examining the effects of feeding omega-3 rich diets to two groups with distinct, genetically determined traits to model different body types and metabolic responses of humans. One group developed obesity more easily and the second was a leaner variety.
When scientists measured changes to the metabolic responses, results showed the omega-3 rich diet reduced cholesterol and improved insulin action and fat metabolism in both groups of mice. However, the obesity prone mice responded less well than the leaner variety, drawing attention to genetically determined pathways that contribute to obesity...
Antibiotics Could Be Driving Up Obesity
The human gut is home to a galaxy of bacteria thought to protect us from disease in the digestive tract and beyond. So what happens when we take antibiotics?
Sure, the pills can wipe out bad bacteria. But they also kill the good stuff. On top of fueling a rise in antibiotic-resistant superbugs, they could be permanently changing the gut environment — a feat some experts fear might be making us fat.
Dr. Martin Blaser of New York University Langone Medical Center studies the effects of antibiotics on Helicobacter pylori — a bacterium that lives quietly in most but leads to ulcers in some.
Although the majority of H. pylori infections are harmless, doctors are quick to treat them with antibiotics that change the way the stomach works.
“Antibiotics are miraculous,” Blaser told ABCNews.com in August after publishing an editorial on antibiotic overuse. “They’ve changed health and medicine over the last 70 years. But when doctors prescribe antibiotics, it is based on the belief that there are no long-term effects. We’ve seen evidence that suggests antibiotics may permanently change the beneficial bacteria that we’re carrying.”
Blaser discussed his latest research with the New York Times, explaining that antibiotics for H. pylori trick the body into eating more by disrupting hunger hormone levels. Indeed, mice given antibiotics get fatter than their untreated counterparts despite having the same diet, Blaser said.
The findings add weight to studies that have found differences in gut bacteria between lean and obese mice. Changes in gut bacteria – called the microbiome – could also be a risk factor for allergies, asthma and diabetes...
Sure, the pills can wipe out bad bacteria. But they also kill the good stuff. On top of fueling a rise in antibiotic-resistant superbugs, they could be permanently changing the gut environment — a feat some experts fear might be making us fat.
Dr. Martin Blaser of New York University Langone Medical Center studies the effects of antibiotics on Helicobacter pylori — a bacterium that lives quietly in most but leads to ulcers in some.
Although the majority of H. pylori infections are harmless, doctors are quick to treat them with antibiotics that change the way the stomach works.
“Antibiotics are miraculous,” Blaser told ABCNews.com in August after publishing an editorial on antibiotic overuse. “They’ve changed health and medicine over the last 70 years. But when doctors prescribe antibiotics, it is based on the belief that there are no long-term effects. We’ve seen evidence that suggests antibiotics may permanently change the beneficial bacteria that we’re carrying.”
Blaser discussed his latest research with the New York Times, explaining that antibiotics for H. pylori trick the body into eating more by disrupting hunger hormone levels. Indeed, mice given antibiotics get fatter than their untreated counterparts despite having the same diet, Blaser said.
The findings add weight to studies that have found differences in gut bacteria between lean and obese mice. Changes in gut bacteria – called the microbiome – could also be a risk factor for allergies, asthma and diabetes...
Red wine has health benefits for obese men, study finds
For the first time, a study has proved that the active ingredient in red wine does make obese men significantly healthier.
“I was happily surprised with the findings,” lead author Patrick Schrauwen told the Star on Tuesday.
“The results were above expectations.”
After 30 days in a random, double-blind study, the obese men who were given 150 milligrams a day of resveratrol showed all the health benefits that come with a calorie-reduced diet and endurance training, Schrauwen said.
Their systolic blood pressure was lower, their mean arterial pressure fell, the fat levels in their livers and muscles dropped and their energy metabolism improved significantly, the study said.
Previous studies on mice showed health benefits from resveratrol, found in red wine and grapes...
“I was happily surprised with the findings,” lead author Patrick Schrauwen told the Star on Tuesday.
“The results were above expectations.”
After 30 days in a random, double-blind study, the obese men who were given 150 milligrams a day of resveratrol showed all the health benefits that come with a calorie-reduced diet and endurance training, Schrauwen said.
Their systolic blood pressure was lower, their mean arterial pressure fell, the fat levels in their livers and muscles dropped and their energy metabolism improved significantly, the study said.
Previous studies on mice showed health benefits from resveratrol, found in red wine and grapes...
Drug Devised to Reduce Obesity
Journal Science Translational Medicine published research has revealed that the US researchers have devised a drug, Adipotide, which has proved success among obese monkeys and mice.
Co-Lead researcher, Professor Renata Pasqualini was of the view that before experimenting drug on rhesus monkeys, they conducted experiment on obese mice. It was found that mice were able to lose 30% of their body weight.
It was only after the success of pre-clinical testing that they decided to have clinical test on rhesus monkeys. After the drug was given to them, it was found that they were able to reduce 11% of their body weight, and also reduced their increased waist line and their BMI also declined...
Co-Lead researcher, Professor Renata Pasqualini was of the view that before experimenting drug on rhesus monkeys, they conducted experiment on obese mice. It was found that mice were able to lose 30% of their body weight.
It was only after the success of pre-clinical testing that they decided to have clinical test on rhesus monkeys. After the drug was given to them, it was found that they were able to reduce 11% of their body weight, and also reduced their increased waist line and their BMI also declined...
Sunday, October 09, 2011
New study suggests inflammation may not be cause of obesity-type 2 diabetes link
For years, it has been assumed that obesity led to type 2 diabetes by causing inflammation, which was thought to change the way the body reacts to the effects of insulin. However, a new study suggests that this hypothesis may need an update.
Researchers from Children’s Hospital Boston reported in the journal Nature Medicine that inflammation actually activates two different proteins that play key roles in stablizing blood sugar levels. Without the presence of inflammation, these proteins remain dormant.
The findings suggest an important new role for inflammation in the body. Rather than being the cause of health problems like type 2 diabetes, heart disease and certain cancers, it may actually be a helpful reaction to other conditions in the body that are the real cause of disease...
Researchers from Children’s Hospital Boston reported in the journal Nature Medicine that inflammation actually activates two different proteins that play key roles in stablizing blood sugar levels. Without the presence of inflammation, these proteins remain dormant.
The findings suggest an important new role for inflammation in the body. Rather than being the cause of health problems like type 2 diabetes, heart disease and certain cancers, it may actually be a helpful reaction to other conditions in the body that are the real cause of disease...
Cold mice might be skewing weight-loss drug studies
Animals and people burn calories in an effort to keep warm, and room temperature may be affecting the testing and development of weight-loss drugs, says University of Alabama at Birmingham researcher Daniel Smith, Ph.D.
Smith, an instructor in the Department of Nutrition Sciences, received a 2011 Early-Career Research Grant from The Obesity Society for his proposal to examine the effect of room temperature on obesity-related drug effects in mice.
“More than 90 percent of weight-loss drugs that show promising results in lab tests fail to reach approval for treatment in humans,” said Smith. “There appears to be a translation gap from the bench to the market. I think the temperature used in animal research facilities may be part of the reason.”
Smith noted that most animals are tested in rooms where the temperature is near 22 degrees Celsius (72F), which is comfortable for most adult humans. However, that temperature is cold for mice, which have to eat more to elevate their metabolic rate to meet the constant, cold stress.
“If you raise the temperature to 30 degrees Celsius, that puts the mice in their thermo-neutral zone or a comfortable temperature for them, mimicking more closely what humans experience in modern daily life,” said Smith.
Smith will test a handful of weight-loss drugs in a group of mice housed at 22 degrees Celsius and another group at 30 degrees Celsius. Food intake, body weight and body composition will be measured to determine drug-related, weight-loss effects in the two temperatures. He said this study could be an important turning point for obesity researchers using animal models.
“This could change the models of pre-clinical drug testing,” said Smith...
Smith, an instructor in the Department of Nutrition Sciences, received a 2011 Early-Career Research Grant from The Obesity Society for his proposal to examine the effect of room temperature on obesity-related drug effects in mice.
“More than 90 percent of weight-loss drugs that show promising results in lab tests fail to reach approval for treatment in humans,” said Smith. “There appears to be a translation gap from the bench to the market. I think the temperature used in animal research facilities may be part of the reason.”
Smith noted that most animals are tested in rooms where the temperature is near 22 degrees Celsius (72F), which is comfortable for most adult humans. However, that temperature is cold for mice, which have to eat more to elevate their metabolic rate to meet the constant, cold stress.
“If you raise the temperature to 30 degrees Celsius, that puts the mice in their thermo-neutral zone or a comfortable temperature for them, mimicking more closely what humans experience in modern daily life,” said Smith.
Smith will test a handful of weight-loss drugs in a group of mice housed at 22 degrees Celsius and another group at 30 degrees Celsius. Food intake, body weight and body composition will be measured to determine drug-related, weight-loss effects in the two temperatures. He said this study could be an important turning point for obesity researchers using animal models.
“This could change the models of pre-clinical drug testing,” said Smith...
Parents' weight affects children, study shows
Overweight parents are more likely to have children who are obese which could lead to the need for weight loss surgery, according to a new study.
Thinner children are therefore more likely to come from slimmer families, researchers at University College London (UCL) have found through a national health survey for England.
Published in the Archives of Pediatrics & Adolescent Medicine, the study found that there is a strong association between children's and parents' body size.
When both parents were in the thinner half of the healthy weight range, the chance of the child being thin was 16.2 per cent, compared with 7.8 per cent when both parents were in the upper half of range.
In comparison, 5.3 per cent of children with two overweight parents are likely to be thin.
Lead author Dr Katriina Whitaker, UCL epidemiology and public health specialist, commented: "We know from other studies that children's weights are correlated with those of their parents, but previous research has tended to focus on obesity rather than the other end of the spectrum."
A further study published in Obesity suggested that green tea could decrease the risk of obesity after lab tests on mice showed positive results...
Thinner children are therefore more likely to come from slimmer families, researchers at University College London (UCL) have found through a national health survey for England.
Published in the Archives of Pediatrics & Adolescent Medicine, the study found that there is a strong association between children's and parents' body size.
When both parents were in the thinner half of the healthy weight range, the chance of the child being thin was 16.2 per cent, compared with 7.8 per cent when both parents were in the upper half of range.
In comparison, 5.3 per cent of children with two overweight parents are likely to be thin.
Lead author Dr Katriina Whitaker, UCL epidemiology and public health specialist, commented: "We know from other studies that children's weights are correlated with those of their parents, but previous research has tended to focus on obesity rather than the other end of the spectrum."
A further study published in Obesity suggested that green tea could decrease the risk of obesity after lab tests on mice showed positive results...
Carbs may suppress fat absorption and accumulation: Animal data
Dietary fructooligosaccharides – carbohydrates with established prebiotic activity – may suppress high-fat diet-induced body fat accumulation, and inhibit intestinal absorption of dietary fats, say researchers.
Writing in the journal BioFactors, researchers investigated the effects of fructooligosaccharides (FOS) on the development of obesity, using two experiments in rats and mice. They found that body weight and percent body fat were lower in mice fed FOS than in controls, whilst rats receiving an oral dose of FOS were reported to have suppressed elevation of plasma triglycerides.
“We have shown that a low dose of dietary FOS suppressed weight gain, accumulation of visceral adipose [fat] tissue, and the increase in liver triglycerides resulting from feeding a high-fat ‘western’ diet ... while fat excretion increased,” reported the authors, led by Yuko Nakamura from the Food and Health R&D Laboratories at the Japanese pharmaceutical company Meiji Seika Kaisha.
“These results suggest that FOS may prevent fat accumulation by inhibiting intestinal absorption of dietary fat in a high-fat ‘western’ diet,” added the researchers...
Writing in the journal BioFactors, researchers investigated the effects of fructooligosaccharides (FOS) on the development of obesity, using two experiments in rats and mice. They found that body weight and percent body fat were lower in mice fed FOS than in controls, whilst rats receiving an oral dose of FOS were reported to have suppressed elevation of plasma triglycerides.
“We have shown that a low dose of dietary FOS suppressed weight gain, accumulation of visceral adipose [fat] tissue, and the increase in liver triglycerides resulting from feeding a high-fat ‘western’ diet ... while fat excretion increased,” reported the authors, led by Yuko Nakamura from the Food and Health R&D Laboratories at the Japanese pharmaceutical company Meiji Seika Kaisha.
“These results suggest that FOS may prevent fat accumulation by inhibiting intestinal absorption of dietary fat in a high-fat ‘western’ diet,” added the researchers...
Discover Key Protein Responsible for Fat Storage
UC Davis Health System researchers have discovered that a protein called galectin-12 plays a key role in fat storage, a finding that could lead to improvements in treating obesity and diabetes. The researchers found that without the ability to make the protein, mice used in their research investigation stored 40 percent less body fat and had increased fat metabolism and decreased insulin resistance.
"This study for the first time demonstrates the importance of a galectin in energy metabolism," said Fu-Tong Liu, distinguished professor and chair of the UC Davis Department of Dermatology, and senior author on the paper.
The findings, published online this week in the early edition of the Proceedings of the National Academy of Sciences, point to galectin-12 as a potential target for the treatment of obesity and diabetes in humans. The breakdown and storage of fat in the body are both tightly controlled processes that involve numerous chemical signals, Liu said.
"In this case, galectin-12 seems to be signaling to fat cells that its time to conserve rather than burn energy," he said. "If we can interrupt that signal, we have a chance at improving fat metabolism and reducing insulin resistance in patients with obesity and type 2 diabetes."
Obesity is the number-one predictor for the development of diabetes, a leading cause of death and disability in the United States. An estimated 24 million Americans have the disease. Between 90 and 95 percent of them have type 2 diabetes, and about 80 percent of people with type 2 diabetes are overweight or obese.
In its early stages, type 2 diabetes is characterized by insulin resistance. The pancreas is producing insulin, but for unknown reasons the body cannot use the insulin effectively. After several years, insulin production decreases, glucose builds up in the blood and the body cannot make efficient use of its main source of fuel. People with advanced diabetes may experience blindness, require limb amputations or suffer fatal organ failure.
In order to discover potential treatments for type 2 diabetes, Liu and his UC Davis colleagues have been working to understand the chemical signals involved in normal energy metabolism and storage. They isolated and cloned the galectin-12 gene 10 years ago. Since then, their studies have shown that the gene is preferentially expressed in fat cells, and that its expression is required for fat-cell differentiation. To enable a focus on specific biological mechanisms associated with galectin-12, the researchers worked with the UC Davis Mouse Biology Program to obtain genetically customized mice that have had individual genes systematically turned off or "knocked out."
"We decided to create the galectin-12 knockout mice to further clarify the function of this protein in animals," said Ri-Yao Yang, associate project scientist...
"This study for the first time demonstrates the importance of a galectin in energy metabolism," said Fu-Tong Liu, distinguished professor and chair of the UC Davis Department of Dermatology, and senior author on the paper.
The findings, published online this week in the early edition of the Proceedings of the National Academy of Sciences, point to galectin-12 as a potential target for the treatment of obesity and diabetes in humans. The breakdown and storage of fat in the body are both tightly controlled processes that involve numerous chemical signals, Liu said.
"In this case, galectin-12 seems to be signaling to fat cells that its time to conserve rather than burn energy," he said. "If we can interrupt that signal, we have a chance at improving fat metabolism and reducing insulin resistance in patients with obesity and type 2 diabetes."
Obesity is the number-one predictor for the development of diabetes, a leading cause of death and disability in the United States. An estimated 24 million Americans have the disease. Between 90 and 95 percent of them have type 2 diabetes, and about 80 percent of people with type 2 diabetes are overweight or obese.
In its early stages, type 2 diabetes is characterized by insulin resistance. The pancreas is producing insulin, but for unknown reasons the body cannot use the insulin effectively. After several years, insulin production decreases, glucose builds up in the blood and the body cannot make efficient use of its main source of fuel. People with advanced diabetes may experience blindness, require limb amputations or suffer fatal organ failure.
In order to discover potential treatments for type 2 diabetes, Liu and his UC Davis colleagues have been working to understand the chemical signals involved in normal energy metabolism and storage. They isolated and cloned the galectin-12 gene 10 years ago. Since then, their studies have shown that the gene is preferentially expressed in fat cells, and that its expression is required for fat-cell differentiation. To enable a focus on specific biological mechanisms associated with galectin-12, the researchers worked with the UC Davis Mouse Biology Program to obtain genetically customized mice that have had individual genes systematically turned off or "knocked out."
"We decided to create the galectin-12 knockout mice to further clarify the function of this protein in animals," said Ri-Yao Yang, associate project scientist...
Gene clue to diabetes sufferers
Scientists have identified a gene that could explain why some people are more susceptible than others to diabetes.
The gene, found in tests on obese mice, controls a protein called tomosyn-2 which acts as a brake on insulin secretion from the pancreas, the researchers also discovered.
Insulin is made and released by beta cells in the pancreas and regulates blood sugars. Those with type 1 diabetes have too little insulin, while those with type 2 are insulin-resistant - both conditions potentially causing serious health problems if they are not treated.
Alan Attie, of the University of Wisconsin-Madison, who led the study, said: "It's too early for us to know how relevant this gene will be to human diabetes, but the concept of negative regulation is one of the most interesting things to come out of this study and that very likely applies to humans."
The researchers studied obese mice as it takes more insulin to lower glucose for an obese person than someone of a healthy weight...
The gene, found in tests on obese mice, controls a protein called tomosyn-2 which acts as a brake on insulin secretion from the pancreas, the researchers also discovered.
Insulin is made and released by beta cells in the pancreas and regulates blood sugars. Those with type 1 diabetes have too little insulin, while those with type 2 are insulin-resistant - both conditions potentially causing serious health problems if they are not treated.
Alan Attie, of the University of Wisconsin-Madison, who led the study, said: "It's too early for us to know how relevant this gene will be to human diabetes, but the concept of negative regulation is one of the most interesting things to come out of this study and that very likely applies to humans."
The researchers studied obese mice as it takes more insulin to lower glucose for an obese person than someone of a healthy weight...
Green Tea May Help You Lose Weight
Drinking green tea can slow down weight gain by limiting the amount of fat absorbed by the body, the Daily Mail reported Wednesday.
In a new study, Penn State University researchers found that a compound in the herbal tea slowed down weight gain in mice.
Crucially, the mice were already obese at the start of the experiment. This makes the findings more relevant to humans because people often consider dietary changes only when they notice problems associated with obesity, the researchers said...
In a new study, Penn State University researchers found that a compound in the herbal tea slowed down weight gain in mice.
Crucially, the mice were already obese at the start of the experiment. This makes the findings more relevant to humans because people often consider dietary changes only when they notice problems associated with obesity, the researchers said...
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