Sunday, September 23, 2012
Study finds that natural killer T-cells in fat tissue guard against obesity
Invariant natural killer T-cells (iNKT) are a unique subset of immune cells that are known to influence inflammatory responses. Now, a scientific team led by researchers at Beth Israel Deaconess Medical Center (BIDMC) has found that iNKT cells play a protective role in guarding against obesity and the metabolic syndrome, a major consequence of obesity.
Their discovery, published on-line today in the journal Immunity, also finds that although iNKT cells are lost when humans become obese, they can be restored through weight loss, and further suggests that therapies that activate iNKT cells could help manage obesity, diabetes and metabolic disease.
iNKT cells had been thought to be rare in humans until work by Lydia Lynch, PhD, found they were plentiful in human adipose (fat) tissue.
"Our previous work had revealed a large population of iNKT cells in fat tissue in both mice and humans,"...
Study: High-fat diet can prevent obesity in mice
In completely counter-intuitive research, scientists at the Hebrew University have found that high-fat meals served at the same time and for the same length of time every day can “reset” metabolism and prevent obesity – that is, at least in laboratory mice....
Drinking green tea helps prevent obesity - study confirms
Drinking green tea helps prevent obesity or weight loss, which is known for some time. A new laboratory study in the Food and Agricultural Chemistry has confirmed the notion that green tea prevents obesity.
M. Ueda and H. Ashida of Graduate School of Agricultural Science, Kobe University in Kobe, Hyogo, Japan tested the expression levels of obesity-related proteins in mesenteric white adipose tissue from C5BL/6 mice fed a high fat diet....
M. Ueda and H. Ashida of Graduate School of Agricultural Science, Kobe University in Kobe, Hyogo, Japan tested the expression levels of obesity-related proteins in mesenteric white adipose tissue from C5BL/6 mice fed a high fat diet....
U of A research could lead to obesity treatment breakthrough
New University of Alberta research — only yet done on mice — has shown a new gene therapy could one day help obese people lose weight, become more active and fight Type 2 diabetes....
Brain neurons and diet influence onset of obesity and diabetes in mice
A lack of AgRP-neurons, brain cells known to be involved in the control of food intake, leads to obesity if mice are fed a regular carbohydrate diet. However, animals that are deficient in AgRP-neurons but which are raised on a high-fat diet are leaner and healthier. The differences are due to the influence of the AgRP-neurons on the way other tissues in the body break down and store nutrients. Mice lacking AgRP-neurons adapt poorly to a carbohydrate diet and their metabolism seems better suited for feeding on fat.
"Susceptibility to obesity and other metabolic diseases is mostly thought to be due to complex genetic interactions and the radical environmental changes that have occurred during the last century. However, it is not just a question of what you eat and your genetic makeup but also how the body manages to convert, store and use food nutrients," commented Serge Luquet, lead author of the study and a researcher at the French Centre National de la Recherche Scientifique (CNRS) Unit of Functional and Adaptive Biology, Université Paris Diderot, Sorbonne Paris Cité...
"Susceptibility to obesity and other metabolic diseases is mostly thought to be due to complex genetic interactions and the radical environmental changes that have occurred during the last century. However, it is not just a question of what you eat and your genetic makeup but also how the body manages to convert, store and use food nutrients," commented Serge Luquet, lead author of the study and a researcher at the French Centre National de la Recherche Scientifique (CNRS) Unit of Functional and Adaptive Biology, Université Paris Diderot, Sorbonne Paris Cité...
New Target for Obesity-Related Disorders
Inhibiting a microRNA that is overexpressed in obese mice and human patients with nonalcoholic fatty liver disease (NAFLD) and type II diabetes could provide a new approach to treating metabolic disorders and even potentially cancer, scientists claim. A team at the University of Illinois at Urbana–Champaign has shown that treating obese mice with an antisense inhibitor of miR-34a corrects the obesity-related abnormal expression of metabolic genes involved in bile acid, glucose, and fat metabolism, and led to reduced liver fat levels and the restoration of glycogen levels and insulin sensitivity...
Sunday, August 19, 2012
Slim down with a shot: Scientists studying obesity vaccine
Could America's obesity epidemic be solved with a vaccine? A newly released study concluded that it could be possible.
The new experimental vaccine targets a hormone known to slow metabolism and cause weight gain. When tested on obese mice, studies showed they lost about 10 percent of their weight in just four days...
The new experimental vaccine targets a hormone known to slow metabolism and cause weight gain. When tested on obese mice, studies showed they lost about 10 percent of their weight in just four days...
Experimental Drug Suppresses Appetite in Mice: Study
An experimental drug tested in mice might one day help people lose weight and keep it off long-term, according to researchers.
The drug, called JD5037, increases sensitivity to the hormone leptin, a natural appetite suppressant found in the body, according to a study in the July 26 issue of the journal Cell Metabolism.
"By sensitizing the body to naturally occurring leptin, the new drug could not only promote weight loss, but also help maintain it," senior study author George Kunos, of the U.S. National Institute on Alcohol Abuse and Alcoholism, said in a journal news release. "This finding bodes well for the development of a new class of compounds for the treatment of obesity and its metabolic consequences."
Leptin supplements alone are not effective at helping people lose excess weight, according to the release. It's believed that this is due to desensitization to leptin, which means that the body can no longer respond to leptin.
In this study, the researchers found that JD5037 suppressed the appetite of obese mice and led to weight loss, in part by resensitizing the mice to leptin...
The drug, called JD5037, increases sensitivity to the hormone leptin, a natural appetite suppressant found in the body, according to a study in the July 26 issue of the journal Cell Metabolism.
"By sensitizing the body to naturally occurring leptin, the new drug could not only promote weight loss, but also help maintain it," senior study author George Kunos, of the U.S. National Institute on Alcohol Abuse and Alcoholism, said in a journal news release. "This finding bodes well for the development of a new class of compounds for the treatment of obesity and its metabolic consequences."
Leptin supplements alone are not effective at helping people lose excess weight, according to the release. It's believed that this is due to desensitization to leptin, which means that the body can no longer respond to leptin.
In this study, the researchers found that JD5037 suppressed the appetite of obese mice and led to weight loss, in part by resensitizing the mice to leptin...
An apple peel a day keeps fat away
Ursolic acid - a waxy substance found in apple peel - increases muscle and brown fat in mice that are on a high-fat diet.
These mice burn more calories and have reduced obesity levels, pre-diabetes and fatty liver disease than the mice that do not receive the supplement. Researhers believe that this might be helpful in reducing obesity...
These mice burn more calories and have reduced obesity levels, pre-diabetes and fatty liver disease than the mice that do not receive the supplement. Researhers believe that this might be helpful in reducing obesity...
Root Cause Discovered for Obesity, Atherosclerosis; PhenObestin 37.5 Can Help
Researchers from the Institute of Molecular and Cell Biology (IMCB) and Singapore Bioimaging Consortium (SBIC) proved that the same gene allowed mice to gain weight and develop atherosclerosis, a progressive disease of the large arteries. Mice that lacked this gene resisted gaining weight or developing atherosclerosis. The groundbreaking research was published in the July 3 issue of Cell Metabolism.
In both obesity and atherosclerosis, lipid droplets accumulate in fat cells. The mice lacking in the crucial gene did not accumulate lipid droplets in their fat cells. The mechanism by which this occurred appeared to be related to the body’s natural autophagy process of degrading undesired cellular components...
In both obesity and atherosclerosis, lipid droplets accumulate in fat cells. The mice lacking in the crucial gene did not accumulate lipid droplets in their fat cells. The mechanism by which this occurred appeared to be related to the body’s natural autophagy process of degrading undesired cellular components...
New Target for Treating Diabetes and Obesity
Researchers at Washington University School of Medicine in St. Louis have identified a potential target for treating diabetes and obesity.
Studying mice, they found that when the target protein was disabled, the animals became more sensitive to insulin and were less likely to get fat even when they ate a high-fat diet that caused their littermates to become obese...
Studying mice, they found that when the target protein was disabled, the animals became more sensitive to insulin and were less likely to get fat even when they ate a high-fat diet that caused their littermates to become obese...
Neutrophils help kick off insulin resistance in obesity
Experts have found that neutrophils play an important role in initiating the chronic inflammation that characterizes obesity-induced insulin resistance.
"These results are largely unexpected," said co-author Day Young Oh, from the University of California in San Diego, USA, in a press statement. "Although several immune cells have been established in the etiology of insulin resistance, the role of neutrophils in this process has remained unclear until now."
The team determined the time course of neutrophil infiltration in the adipose tissue of mice fed a high-fat diet (HFD), using fluorescence-activated cell sorting to identify adipose tissue neutrophils (ATNs).
As reported in Nature Medicine, there was a rapid increase in ATN levels after just 3 days of HFD feeding and ATN content remained elevated 12 weeks into the diet. Similarly, the expression of neutrophil elastase, a protease secreted by neutrophils, was significantly increased 3 days into the HFD and remained elevated after 12 weeks.
Consistent with these findings, neutrophil elastase activity was also significantly higher in the HFD mice after 12 weeks than it was in mice fed standard chow...
"These results are largely unexpected," said co-author Day Young Oh, from the University of California in San Diego, USA, in a press statement. "Although several immune cells have been established in the etiology of insulin resistance, the role of neutrophils in this process has remained unclear until now."
The team determined the time course of neutrophil infiltration in the adipose tissue of mice fed a high-fat diet (HFD), using fluorescence-activated cell sorting to identify adipose tissue neutrophils (ATNs).
As reported in Nature Medicine, there was a rapid increase in ATN levels after just 3 days of HFD feeding and ATN content remained elevated 12 weeks into the diet. Similarly, the expression of neutrophil elastase, a protease secreted by neutrophils, was significantly increased 3 days into the HFD and remained elevated after 12 weeks.
Consistent with these findings, neutrophil elastase activity was also significantly higher in the HFD mice after 12 weeks than it was in mice fed standard chow...
Protein Fights Obesity, Diabetes
A protein that slows aging in mice and other animals also protects against the ravages of a high-fat diet, including diabetes, according to a new MIT study.
MIT biology professor Leonard Guarente discovered SIRT1’s longevity-boosting properties more than a decade ago and has since explored its role in many different body tissues. In his latest study, appearing in today’s print edition of the journal Cell Metabolism, he looked at what happens when the SIRT1 protein is missing from adipose cells, which make up body fat.
When put on a high-fat diet, mice lacking the protein started to develop metabolic disorders, such as diabetes, much sooner than normal mice given a high-fat diet...
MIT biology professor Leonard Guarente discovered SIRT1’s longevity-boosting properties more than a decade ago and has since explored its role in many different body tissues. In his latest study, appearing in today’s print edition of the journal Cell Metabolism, he looked at what happens when the SIRT1 protein is missing from adipose cells, which make up body fat.
When put on a high-fat diet, mice lacking the protein started to develop metabolic disorders, such as diabetes, much sooner than normal mice given a high-fat diet...
Hormone Levels Linked To Metabolic Disease
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...
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...
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...
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