WELCOME!

Welcome to the Turn Fat People Into Mice blog. (Note size comparison of fat mouse with a 747)

I have started this very important blog and will update it regularly.

It offers timely posts documenting the cutting edge science re: rodentia obesus and the world's growing knowledge of how to make fat mice thin.

"In labs, we've cured obesity and diabetes in mice hundreds of times," Smith said.

Though most successful fat research appears to be on mice, we are an equal opportunity site and do not discriminate against any rodent.

Therefore, for example, if research turning fat rats into thin rats comes to our attention, we will let you know about it.

We will even support turning fat people into rats, for example, if that's what it takes to help them.

It is important to have a searchable and accessible whole planet repository of the research that demonstrates our unparalleled ability to turn fat mice into thin mice.

Since we are experts at fixing fat mice, instead of trying to work it out for humans, where there are apparently at least 6000 genes relating to overweight/obesity, let's research how to turn fat people into mice.

"Scientists think that the mouse genome will be even important (sic) than the human genome to medicine and human welfare. That seems bizarre: why is that? The reason is that, because of the relatively 'recent' divergence of the mouse and human lineages from our common ancestor (about 75 million years ago), an astonishing 99% of mouse genes turn out to have analogues in humans. Not only that, but great tracts of code are syntenic - that means the genes appear in the same order in the two genomes...

The astonishingly close homology that has been revealed in the code between mouse and human genome extends to functionality. Many homologous genes have identical functions in the two species, anatomy, physiology and metabolism are similar and genetic disease pathology can be very similar. So the fact that we can study the mouse empirically, means that we can identify the functions of genes in people and both understand human disease pathology and create ways to treat it." (source)

Clearly, turning fat people into mice is a simpler matter.

Keep visiting the Turn Fat People Into Mice blog for timely posts documenting the cutting edge science re: rodentia gordo and the world's growing knowledge of how to make fat mice thin.

Fat mouse (lower) vs. skinny mouse:

Obesity cure claim by Irish and US researchers from Trinity and Harvard

Irish scientists believe they have reached a pivotal point in their research into the battle against obesity.

The research carried out by Trinity College Dublin, St Vincent's Hospital and Harvard University found that a type of anti-tumor immune cell protects against obesity and the metabolic syndrome that leads to diabetes.

They have discovered that a lipid, “aGC”, can bring a major improvement to metabolism, weight loss and fatty liver disease. It can also reverse diabetes.

Their results show that immune cells known to be protective against malignancy are lost when people become obese. However they are restored with weight loss.

These invariant natural killer T-cells (iNKT) had been thought to be rare in humans until work found they were plentiful in human omental fat.

Dr. Lydia Lynch is from Trinity College Dublin said “We then found a large population of iNKT cells in fat tissue from mice...

Heat-processed food ups obesity, diabetes risk

Researchers at Mount Sinai School of Medicine have identified a common compound in heat-processed food that could play a major role in the development of abdominal obesity, insulin resistance, and type 2 diabetes.

The research team, led by Helen Vlassara, MD, Professor and Director of the Division of Experimental Diabetes and Aging, found that mice with sustained exposure to the compound, methyl-glyoxal (MG), developed significant abdominal weight gain, early insulin resistance, and type 2 diabetes....

Super Muscular Mice Could Help Treat Diabetes, Make You Buff

Researchers can make Mighty Mice by tinkering with their proteins before they are born, a new study suggests. These super mice have bigger and stronger muscles than their normal counterparts later in life.

The protein the researchers blocked, called Grb10, seems to regulate muscle development, since the researchers only changed the protein while the mice were in the womb. When they turned off the protein during development, the researchers saw more muscle and stronger muscle in the mice when they become adults.

They found that, instead of larger muscle fibers, the mice had a greater number of muscle fibers — the individual segments that make up the muscles.

The finding actually comes out of a diabetes and obesity research program — this protein responds to insulin signals, and muscularity seems to go along with other traits that seem to protect a person from diabetes. These include how the body handles sugars and fats and how well it responds to insulin....

How 'beige' fat makes the pounds melt away

Researchers from the University of Bonn and the Max Planck Institute of Biochemistry in Martinsried have decoded a signal path that could boost the burning of body fat. Mice that are missing a signal switch called VASP are clearly leaner and have more of the coveted brown and beige-colored fat cells that convert energy into heat. This might point the way to a new method for fighting obesity. The researchers presented their results in the current issue of the renowned journal Science Signaling.


The numbers of obese people are climbing steeply all over the world – with obvious major consequences for their health. Due to excess food intake and a lack of physical activity, but also due to genetic factors, the risk for overweight people dying from diseases like coronary heart disease, diabetes und atherosclerosis increases. "The body's fat reserves are actually used as a place to store energy that allows surviving lean times," says Prof. Dr. Alexander Pfeifer, Director of the Institute of Pharmacology and Toxicology of the University of Bonn. "But nowadays, hardly anyone in the industrialized nations is exposed to such hunger phases anymore."


A signal path boosts the burning of fat in the body


Since many people ingest more energy in their diet than they can burn, many harbor dreams of a magic pill that will simply make fat melt away. Now, scientists around Prof. Pfeifer – in collaboration with colleagues from Epileptology and from the PharmaCenter Bonn, together with the Max Planck Institute of Biochemistry in Martinsried - have discovered a signal path in the metabolism of mice that is indeed able to greatly boost combustion inside the rodents' bodies....

Antibiotic use in early life linked to obesity

A new study has confirmed the theory that low doses of antibiotic drugs may alter the composition and function of the bacteria in the gut, causing weight gain through changes in metabolism.

Researchers administered sub-therapeutic antibiotic therapy to mice and a control group. After approximately six weeks, the mice receiving antibiotics had gained around 10% to 15% more fat mass than the mice not receiving antibiotics....

Tackling obesity by manipulating gut flora

Antibiotics could one day be the standard treatment for regulating weight, suggests a new study in Nature Immunology that examines the interactions between diet, the bacteria in our gut, and our immune systems.


The 500 different types of bacteria present in our gut provide the enzymes necessary for the uptake of nutrients, synthesize certain vitamins and boost absorption of energy from food. Last century, farmers learned that by tweaking the microbial mix in their livestock with low-dose oral antibiotics, they could accelerate weight gain.

In the new study, researchers at the University of Chicago found they were able to manipulate some of the mechanisms that regulate weight gain. They focused on the relationship between the immune system, gut bacteria, digestion and obesity. Their findings show how weight gain requires not just caloric overload but also a delicate, adjustable - and transmissible - interplay between intestinal microbes and the immune response.

"Diet-induced obesity depends not just on calories ingested but also on the host's microbiome," said the study's senior author Yang-Xin Fu, professor of pathology at the University of Chicago Medical Center. "For most people, host digestion is not completely efficient, but changes in the gut flora can raise or lower digestive efficiency."

In one experiment, the researchers compared normal mice with mice that have a genetic defect that renders them unable to produce lymphotoxin, a molecule that helps to regulate interactions between the immune system and bacteria in the bowel. On a standard diet, both groups of mice maintained a steady weight. But after nine weeks on a high-fat diet, the normal mice increased their weight by one-third, most of it fat. Mice lacking lymphotoxin ate just as much, but did not gain weight....

Study in mice discovers injection of heat-generating cells reduces belly fat

The injection of a tiny capsule containing heat-generating cells into the abdomens of mice led those animals to burn abdominal fat and initially lose about 20 percent of belly fat after 80 days of treatment.


Researchers conducting the study were surprised to see that the injected cells even acted like "missionaries," converting existing belly fat cells into so-called thermogenic cells, which use fat to generate heat.


Over time, the mice gained back some weight. But they resisted any dramatic weight gain on a high-fat diet and burned away more than a fifth of the cells that make up their visceral fat, which surrounds the organs and is linked to higher risk for Type 2 diabetes, cancer and heart disease....

Weird science: Fat capsule injections could make you thinner

This just in from Ohio State University: fat plus more fat equals thin. In other words, if you've been trying to lose weight by adding less fat to your body, you've been doing it all wrong.

Your body stores a couple different kinds of fat. There's white fat, or visceral fat, which is that fatty "fat" fat that you have to be careful of. There is also brown fat, or "good" fat, which is related to muscle and can burn fat to generate heat.

Researchers at Ohio State took a small gel-like capsule full of specially engineered brown fat cells and implanted it into an obese mouse, expecting that the cells in the capsule would start burning fat. What they didn't expect was that the cells in the capsule would act like "missionaries," converting existing white fat cells into brown fat. The result was that the obese mice in the study lost about 20 percent of belly bulge after 80 days, even while continuing to eat excessive saturated fat. There were no immune responses to the implants and no side-effects: the mice just got less fat, and stayed that way, without changing their lifestyle....

No Fat Mice in This Lab

Two microRNAs have been identified as potential therapeutic targets for obesity. Researchers at Virginia Tech and the University of Texas Southwestern Medical Center at Dallas have shown that mice genetically engineered to lack microRNA-378 (miR-378) and miR-378* are remarkably resistant to obesity when fed a high-fat diet, and are metabolically more capable of converting food into energy than wild-type littermates....

Carefully scheduled diets 'combat obesity better than fat reduction'

New research has shown that scheduling food consumption in a way that improves metabolic efficiency could be the best way of preventing obesity.

A team from the Hebrew University of Jerusalem has carried out research using mice which shows that a scheduled high-fat diet can offer greater benefits than an unscheduled low-fat diet with the same number of calories....

Scientists develop herb-based anti-obesity medicine

A group of South Korean scientists has developed a new herb-based medicine that can help prevent and even cure obesity that has also been proven safe, the science ministry said Thursday.

The medicine uses a mixture of substances extracted from perennial plants that are already familiar to oriental medicine, according to the Ministry of Education, Science and Technology.

The new substance, called POCUb, boosts activities by the AMP-activated protein kinase that dissolves body fat while suppressing the activity of an enzyme, known as phosphodiesterase, that causes the accumulation of body fat.

A series of animal tests showed the effectiveness of the new herbal medicine in both preventing and curing obesity, a leading cause of death throughout the world, the developers from the Korea Institute of Oriental Medicine said.

A group of mice treated with the medicine gained up to 61 percent less body weight compared to controlled groups, reflecting the substance's effectiveness in preventing obesity....

Fat fighters found in fat tissue

Researchers at Harvard-affiliated Beth Israel Deaconess Medical Center (BIDMC) have found that a type of immune system cell once thought rare in humans is actually plentiful in fat cells and protects against obesity and the metabolic syndrome that leads to diabetes.

Research published online today in the journal Immunity finds that invariant natural killer T-cells (iNKT), immune cells known to influence inflammatory responses, are lost when humans become obese but can be restored through weight loss. The work 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, a research fellow in medicine at Beth Israel, found they were plentiful in human fat, also known as adipose tissue.

“Our previous work had revealed a large population of iNKT cells in fat tissue in both mice and humans,” said Lynch, a research fellow in the Department of Hematology/Oncology at BIDMC and the study’s first author. “Now we have identified them in mice and identified a role for them in the regulation of body weight and the metabolic state, likely by regulating inflammation in adipose tissue.”...

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....

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...

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...

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...

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...

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...

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...

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...

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...

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...

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...

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...

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...

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...

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...

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...

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...

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...

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...

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.