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.

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

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

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

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...

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...

'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...

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...

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.'...

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.

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...

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...

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...

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...

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...

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...

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...

‘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...

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...

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...

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...

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...

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...

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...

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...

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...

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...

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...

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...

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...

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.

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...

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...

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...

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.

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...

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...

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...

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...

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...

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...

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...

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...

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...

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...

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...

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...

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...

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...

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...

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...

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...

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...

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...

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...

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...

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...

Scientists identify genes involved in storing fat

Researchers funded by the Wellcome Trust have identified several genes in fat tissue that may lead us to retain fat unnecessarily in the body. The study, using a mouse model, may explain why some people carry more weight than others even when they have similar diets because of genes that encourage fat storage.

Scientists at the University of Edinburgh compared fat tissue from mice that had been selectively bred for many generations to be increasingly fat or thin, and as a result had acquired weight-related genes. The research, published in the journal ’PLoS One’, cross-referenced thousands of genes and pinpointed genes that prevented the breakdown of fat, which were more prevalent in the fat tissue of the overweight mice than in the fat tissue of the lean mice.

Mice were then bred from one overweight parent and one lean parent. Those among the offspring that were born overweight were found to have the same active genes as the fatter parent mice - an indication that hereditary factors play a part in fat storage and can increase the likelihood of putting on weight.

The research also found that the thin offspring had an added protection against weight gain. When both sets of mice were given fatty foods, the thin offspring seemed able to break down fatty tissue more easily than the heavier mice, suggesting they had inherited ’lean genes’...

Fat content in mice affected by environment

A recent study found that mice living in socially enriching environments converted a greater portion of their energy-storing white fat to energy-burning brown fat, losing weight despite their increased caloric intake. These findings reinforce how social and physical environments can impact animal metabolisms.

Adipose tissue, commonly known as fat, comes in two types: white and brown. White fat, which constitutes as much as 20 percent of the body weight in men and 25 percent of the body weight in women, serves to store excess energy, cushion organs and maintain body temperature. Brown fat, which is especially abundant in newborns and hibernating mammals, expends energy to generate heat. Increases in white fat and brown fat concentrations are associated with weight gain and loss, respectively.

Functional differences between white and brown fat are predicted by differences in structure. White adipocytes contain a single, large lipid droplet that occupies most of the cell volume. In contrast, brown adipocytes contain numerous small droplets, more iron-containing mitochondria, which explains the characteristic brown color, and more capillaries to deliver greater amounts of oxygen.

While brown fat is best known for its role in insulating infants, scientists found that active brown fat is also present in adults. In addition, cold exposure and activation of the sympathetic nervous system drives the production of more brown fat. The new study, whose results are published in the September issue of Cell Metabolism, suggests that an engaging environment can provide another, perhaps more effective means to increase brown fat.

According to Lei Cao of The Ohio State University, the typical laboratory mouse leads what might be considered a "couch potato" lifestyle. Lab mice are given free access to food and water, as well as a few potential playmates. However, they are not given much else to do.

In the enriched environment, mice live in groups of 15 to 20. They are given more space as well as exercise wheels, mazes and toys. After four weeks in the enriched environment, the mice's abdominal fat decreased by 50 percent...

Black tea extract prevents obesity

There are many diets you can try to avoid or prevent obesity. But chances are good that none of them work for you. The problem is that most people couldn't control their daily intake of calories because foods with high fat, high salt and high sugar taste just too good.

New research suggests that simply taking some extract of a Chinese black tea called Pu-Erh tea after meals may help you stop gaining weight even if you continue eating a typical obesity-inducing Western diet full of high fat, high protein and high energy.

The research conducted by Yasuyuki Oi of Nippon Supplement, Inc. based out of Osaka, Japan found mice given the black tea extract in some dose did not raise levels of blood triglycerides after ingestion of a corn oil emulsion.

The researchers published the results in Phytotherapy Research. In the research, female ddy mice were given one of seven diets with either high fat, or a normal dietary composition, or supplemented black tea extract, or gallic acid in different doses for a period of 12 weeks...

Will new wonder drug let humans 'have their cake and eat it, too?'

Imagine a drug that combines an ingredient found in red wine, which extends your life on the provision you eat as much as you please, eventually becoming obese. Sound too good to be true? Those are the provisions of the new drug called SRT-1720, and the success found in obese lab mice has been amazing.

LOS ANGELES, CA (Catholic Online) - SRT-1720 is an experimental agent, which in different forms is also being tested in humans. The drug found to prevent some of the life-shortening diseases associated with obesity in mice, by curbing levels of fat in the liver and improving sensitivity to insulin.

SRT-1720 is based on the compound resveratrol, which is found in red wine and is thought to combat some of the effects of aging by boosting levels of proteins called sirtuins. These are the proteins that have been associated with 30 percent life extension in mice and rats put on low-calorie diets.

Developed by David Sinclair, a biologist at Harvard Medical School and one of the co-authors of the current mouse study, the findings associated with SRT-1720 appear in the new journal Scientific Reports...

Slim down by targeting the hormone uroguanylin

The number of people who are obese and suffer one or more of its associated health problems (including type 2 diabetes) is escalating dramatically. Researchers are seeking to identify new targets for therapeutics that could limit appetite and thereby obesity. A team of researchers, led by Scott Waldman, at Thomas Jefferson University, Philadelphia, has now uncovered one such potential target by studying the molecular control of appetite in mice.

In the study, Waldman and colleagues found that nutrient intake by mice caused cells in their gut to secrete the precursor of the hormone uroguanylin (prouroguanylin) into the blood...

Genetics' new frontier: What mom eats, weighs in pregnancy can set child up for obesity, diabetes

Cracking the human genome is already old news for those riding the next wave of genetic research. The rising field of epigenetics is revealing how diet, behavior and the environment are reprogramming the genes we're dealt at conception.

Although your DNA was locked in the moment your parents' egg and sperm met, how those genes get expressed depends on what happened next. "Most chronic diseases that occur in adulthood have their origins in the first 1,000 days after conception," said Kent Thornburg, an epigenetics researcher at Oregon Health and Science University.

What's more, the epigenetic changes that happen in the womb get passed on to future generations.

Sorry, moms. That means once again, the pressure is on you.

"If your mom was obese while she was pregnant with you, you're marked," said Philip Wood, professor at Sanford Burnham Research Institute in Lake Nona. You will have an uphill battle fighting off excess weight and its ill effects, including diabetes and heart disease, even if you're adopted and raised by slim parents, he said.

The findings are significant as medical science works to identify causes and cures for the two most serious and costly epidemics facing America: obesity and diabetes.

We don't understand all of the mechanisms, but they likely involve maternal circulating hormones, such as leptin and insulin, and glucose levels that can alter how the placenta develops and what nutrients cross it, said Tracy Bale, associate professor of neuroscience at the University of Pennsylvania School of Veterinary Medicine, who has done epigenetic studies on animals.

Studies have shown that these effects can be handed down to the next generation, she added.

Rewriting the script

Epigenetics can silence or draw out the expression of genes.

"If DNA is the hardware, epigenetics is the software that tells genes what to do," said Randy Jirtle, an epigenetics researcher at Duke University Medical Center.

A study conducted on mice, and published in 2003 in Molecular Cell Biology, illustrated the effects of diet on genes. The mice in the study carried the agouti gene, which humans also have.

When scientists fed pregnant mice a certain diet that silenced the gene, the baby mice came out yellow, fat and prone to diabetes and cancer. When they fed the mice diets that activated the gene — a diet rich in folic acid, B vitamins and choline — mice came out skinny, brown and not susceptible to disease.

"The mice were genetically identical," said Jirtle, who was part of the study. "The only difference was what the mothers ate."

Granted these are mice, not humans, he added, "but the experiment showed that a mother's diet can shape the epigenome of her offspring."...

How fatty food triggers diabetes: Scientists believe discovery paves way for Type 2 'cure'

Fatty food trips a genetic switch in the body that can trigger diabetes, a study has found.

Understanding the biological pathway could lead to a potential cure for the disease, say scientists.

The discovery helps explain why Type 2 diabetes is so often linked to obesity.

In studies of mice and humans, researchers found that high levels of fat disrupted two key proteins that turn genes on and off...

Fat Mice Live Longer With Novel Drug

An investigational compound extended survival in middle-age, obese male mice that were eating a high-fat diet, but researchers warned that it was too soon to say if the drug could do the same for humans.

Three groups of mice all gained a similar amount of weight during the study, but those that ate a low dose of SRT1720 lived 4% longer and those that ate a high dose lived 18% longer than their untreated counterparts (P<0.001), Rafael de Cabo, PhD, of the National Institute on Aging's Laboratory of Experimental Gerontology in Baltimore, and colleagues, wrote online in Scientific Reports...

Compound improves health, increases lifespan of obese mice

Researchers have reported that obese male mice treated with a synthetic compound called SRT1720 were healthier and lived longer compared to non-treated obese mice. The experimental compound was found to improve the function of the liver, pancreas and heart in mice.

The National Institute on Aging (NIA) supported the study, in collaboration with Sirtris, a GlaxoSmithKline company. The study was primarily conducted by the NIA, part of the National Institutes of Health, and is published online in the Thursday, August 18, 2011, issue of Scientific Reports.

"This study has interesting implications for research on the biology of aging. It demonstrates that years of healthy life can be extended in an animal model of diet-induced obesity by a synthetic compound that modulates a gene pathway associated with aging," said NIA Director Richard J. Hodes, M.D. More research is needed to assess the relevance of these findings in people, Hodes and the researchers noted.

SRT1720, a patented molecule, has been shown to activate the SIRT1enzyme, part of a class of enzymes called sirtuins. Sirtuins have been previously implicated in aging processes and are thought to contribute to the positive effects of dietary restriction (also known as calorie restriction) in higher organisms, including nonhuman primates.

In this study, scientists compared the health of 1-year-old, or middle-aged, male mice fed a high-fat diet with a high dose of SRT1720, a low dose of SRT1720 or no SRT1720. Additionally, these mice were compared to a control group of 1-year-old male mice fed a standard diet...

Brown Fat, Also Known As Good Fat, More Common In Leaner Children

Investigators at Joslin Diabetes Center and Children's Hospital Boston have revealed that a type of "good" fat known as brown fat occurs in varying amounts in children which increases until puberty and then declines. Brown fat is more common in children who are leaner...

In 2010 a Joslin investigation identified cells in mice that can be triggered to transform into brown fat....

Brain Protein ‘Nesfatin-1’ Shows Promise In Checking Obesity

Study conducted by an Indian-origin researcher showed that protein present in human brain may actually hold the key to keeping hunger and blood glucose in hand and keep unwanted pounds away.

Associate professor in biology at Canada's York University, Suraj Unniappan is investigating the metabolic effects of a protein known as nesfatin-1 present within the human brain.

Prof Suraj discovered that rats fed nesfatin-1 consumed less, utilized extra stored fat and turned more active.

In addition, it induced insulin discharge from the pancreatic beta cells of both rats and mice...

York U Researchers Zero In On Protein That May Help Treat Obesity, Diabetes

A newly-identified protein may hold the key to keeping appetite and blood sugar in check, according to a study by York University researchers.

Suraj Unniappan, associate professor in York's Department of Biology, Faculty of Science & Engineering, is delving into the metabolic effects of a protein called nesfatin-1, abundantly present in the brain. His studies found that rats administered with nesfatin-1 ate less, used more stored fat and became more active. In addition, the protein stimulated insulin secretion from the pancreatic beta cells of both rats and mice.

"[The rats] actually ate more frequently but in lesser amounts," says Unniappan, a member of York's neuroscience graduate diploma program, and a recipient of a Canadian Institutes of Health Research (CIHR) New Investigator Award. "In addition, they were more active and we found that their fatty acid oxidization was increased. In other words, the energy reserve being preferably used during nesfatin-1 treatment was fat. This suggests more fat loss, which could eventually result in body weight loss," he says....

Medical: In the obesity battle, it's mind over stomach

...Last winter, Baylor College of Medicine scientists reported working with mice genetically modified to lack a receptor for the ghrelin hormone.

They found this turned up the fat-burning thermostat in the animals' bodies. In an older group of the mice, the rodents were slimmer than a control group even though they ate just as much and were no more physically active.

Still another mouse study, reported in this month's Cell Metabolism, looked more closely at what happens inside the hypothalamus and found that when they are starved, some neurons in that part of the brain actually start eating bits of themselves, which in turn ramps up hormonal signals to start eating.

Such cellular cannibalism goes on all the time as part of the body's natural housekeeping, but the discovery that this process also helps regulate appetite opens a new possible route for obesity-fighting drugs....

A Protein May Help Treat Obesity, Diabetes

A newly-identified protein may hold the key to keeping appetite and blood sugar in check, according to a study by York University researchers.

Suraj Unniappan, associate professor in York's Department of Biology, Faculty of Science & Engineering, is delving into the metabolic effects of a protein called nesfatin-1, abundantly present in the brain. His studies found that rats administered with nesfatin-1 ate less, used more stored fat and became more active. In addition, the protein stimulated insulin secretion from the pancreatic beta cells of both rats and mice.

"[The rats] actually ate more frequently but in lesser amounts," says Unniappan, a member of York's neuroscience graduate diploma program, and a recipient of a Canadian Institutes of Health Research (CIHR) New Investigator Award. "In addition, they were more active and we found that their fatty acid oxidization was increased. In other words, the energy reserve being preferably used during nesfatin-1 treatment was fat. This suggests more fat loss, which could eventually result in body weight loss," he says.

The findings were reported in two recent research articles from Unniappan's laboratory: one published August 9 in Endocrinology and another in March 2011 in Journal of Endocrinology.

Discovered by a research team from Japan in 2006, nesfatin-1 was earlier found to regulate appetite and the production of body fat when injected into the brain of mice and rats...

Mimicking Calorie Restriction to Fight Obesity and Type 2 Diabetes

A Yale University-led research team has discovered how reduced expression of a particular gene protects against obesity and type 2 diabetes, possibly prolonging lifespan by mimicking the effects of calorie restriction. The study appears in the August 3 issue of Cell Metabolism.

It is known that excess calorie consumption leads to obesity, insulin resistance and increased mortality, whereas calorie restriction reduces accumulation of body fat and improves cellular energy balance and insulin action – reversing obesity and type 2 diabetes, delaying the aging process, and prolonging life in primates and many other species.

It has also been shown in the past that reduced expression of the so-called “INDY” gene in D. Melanogaster flies and C. elegans worms promotes longevity in a manner similar to calorie restriction. But until now, the cellular mechanism by which this happens was unknown.

The Yale team generated a mouse with the so-called “INDY” gene deleted. Loss of the gene altered chemical levels in the cellular signaling network in a way that improved mitochondrial action in the liver, metabolism of fatty acids, and cellular energy transport. Overall, these traits protected the mice from diet-related accumulation of body fat and insulin resistance that evolve, as we age, into type 2 diabetes...

Obesity ups risk of diabetes

Scientists at Joslin Diabetes Center have found how obesity drives insulin resistance, the condition that may lead to type 2 diabetes.

They uncovered that excess weight wreaks its havoc by altering the production of proteins that affect how other proteins are spliced together.

The finding may point toward novel targets for diabetes drugs.

Scientists in the lab of Mary-Elizabeth Patti, M.D., began by examining the levels of proteins in the livers of obese people, and finding decreases in number for certain proteins that regulate RNA splicing.


"When a gene is transcribed by the cell, it generates a piece of RNA," stated Dr. Patti, who is also an Assistant Professor of Medicine at Harvard Medical School.

"That piece of RNA can be split up in different ways, generating proteins that have different functions.

"In the case of these proteins whose production drops in the livers of obese people, this process changes the function of other proteins that can cause excess fat to be made in the liver.

"That excess fat is known to be a major contributor to insulin resistance," she explained.

The investigators went on to examine a representative RNA-splicing protein called SFRS10 whose levels drop in muscle and liver both in obese people and in over-fed mice...

Dieting Leads to Self-Cannibalization of the Brain: Study

Dieting makes brain cells eat themselves, researchers said Wednesday.

In a new report, scientists say that hunger-inducing neurons consume themselves for energy during periods of starvation. This causes the body to produce fatty acids, which increases the amount of AgRP in the brain. AgRP is a hunger-signaling peptide that raises the desire to eat.

The study was conducted on lab mice, and published in the journal Cell Metabolism. The metabolic processes between mice and humans are very similar, according to the Los Angeles Times, especially when it comes to feeling hungry...

Krill Oil Reduces Ill Effects of High-Fat Diet

...The study results showed that feeding a high-fat diet to mice compared to animals given a low-fat diet led to an elevation of endocannabinoids (EC), lipid messengers that can activate specific receptors, thereby influencing not only enzyme activities, but also appetite, energy balance, mood, memory, and pain perception. In doing so, the EC system contributes to visceral fat accumulation. Superba krill oil was able to counteract the high fat diet-induced changes in EC levels after eight weeks of treatment. In addition to reducing EC levels in several different tissues, administration of krill oil also exerted lowering effects on triglyceride, cholesterol and a marker of inflammation...

For A Sugary Way Out Of Obesity!

Sugarcane extract could be a pleasant tool in the fight against obesity, Australian researchers believe. The results of the La Trobe University experiments on mice and reported in Nutrition Horizon, may provide a new approach for weight management in humans.


The study was carried out by Dr Richard Weisinger with La Trobe colleagues Dr Lauren Stahl, Dr Denovan Begg, Dr Mark Jois and collaborators Dr Ankur Desai and Dr Jason Smythe from Horizon Science, a Melbourne based food biotechnology firm. Their work was discussed at a meeting of the Society for the Study of Ingestive Behavior held in Clearwater, Florida, USA.

Molasses usually end up as a waste-product of sugar refining. However, they are rich in polyphenols, says Dr Weisinger, chemicals found in plants known for their antioxidant properties.

Researchers supplemented the high-fat diet of a group of laboratory mice with molasses for 12 weeks. They found that these mice had lower body weight, reduced body fat and decreased blood levels of leptin – a hormone involved in energy regulation, appetite and metabolism – than the control group.

Further analyses, says Dr Weisinger, revealed that molasses supplements led to increased energy excretion, i.e, more calories were lost in faeces. They also found increased gene expression for several liver and fat cell biomarkers of energy metabolism...