How Weight-Loss Surgery Reverses Type 2 Diabetes: New Study Offers Explanation

A team of researchers, led by a UC Davis veterinary endocrinologist, has shown for the first time that a surgical procedure in rats that is similar to bariatric surgery in humans can delay the onset of type 2 diabetes. The researchers also have identified biochemical changes caused by the surgeries that may be responsible for that delay...

Why tangy fruit could stop you gaining weight

The secret to staying slim may lie in a tangy fruit.

The juice of the blood orange stops mice piling on weight when fed a high-fat diet, research shows.

In contrast, mice fed sweeter oranges more popular in the UK gain significant amounts of fat.

Scientists believe the fat-busting powers of the fruit, grown in Italy and the U.S., may be partly due to its high levels of anthocyanin. This red pigment that gives the orange its deep colour is a type of antioxidant, a natural chemical that helps ward off disease.

The juice damages the ability of cells called adipocytes to accumulate fat, University of Milan researchers told the International Journal of Obesity.

Adipocytes are found mostly around the waistline and absorb fat from food to store as energy.

Mom’s Obesity Influences Kid’s Weight

Scientists at two ARS-funded nutrition research centers are examining how maternal influences of the unborn child and the developing newborn could increase the risk that the child would become an overweight or obese adult. In turn, that adult would have a higher risk of obesity-related afflictions such as type 2 diabetes or cardiovascular disease...

At the ARS Children’s Nutrition Research Center at Baylor College of Medicine in Houston another researcher is studying the “epigenetic mechanism” link to obesity. The researchers studied a population of genetically similar laboratory mice known for their genetic tendency toward obesity. The findings suggest that “an epigenetic mechanism may act to increase the severity of obesity from one generation to the next.” This “transgenerational amplification of obesity” occurred in three successive generations of mice. Specifically, overweight dams gave birth to even-more-overweight offspring, the females of which gave birth to even heavier pups, and so on, through generation three.

Reported in the International Journal of Obesity, the study showed that the mothers’ obesity apparently induced changes in the expression of genes that control the formation of the pups’ body-weight-regulating mechanisms. That likely took place in the womb and perhaps in the weeks thereafter, setting the pups on the path to obesity.

Scientists Identify Key Protein from Mitochondria in Energy Regulation

With obesity and obesity-related diseases epidemic in the developed world, a clear understanding of how metabolism is regulated is crucial. One of the key metabolic pathways involves the oxidation of fat. In the current edition of the journal Nature, scientists at the Gladstone Institute of Virology and Immunology report on a new mechanism that governs this pathway and in the process identified a novel potential therapeutic target for controlling fat metabolism.

The target is a protein from the mitochondria, or the "power plants" of every cell that are responsible for processing oxygen and converting substances from the foods we eat into energy for essential cell functions.

"Many mitochondrial proteins undergo a small chemical modification known as acetylation, which varies during feeding and fasting conditions," said Eric Verdin, MD, senior investigator and senior author of the study. "From our previous studies, we knew that the enzyme SIRT3 is involved in removing these modifications, and we speculated that SIRT3 might have a role in regulating metabolism and looked for how it might do this."

To study the enzyme's role in mice, the researchers used mice in which both copies of the gene had been deleted. Interestingly, mice that lost both copies of the SIRT3 gene appeared to be completely normal. However, the investigators then tested the mice under fasting conditions. During fasting, expression of SIRT3 was increased in the liver, an organ that helps maintain the body's energy balance. The livers of mice without SIRT3 had higher levels of fat and triglycerides than normal mice, because the mice could not burn fat...

Obesity as protection against metabolic syndrome, not its cause

The collection of symptoms that is the metabolic syndromeinsulin resistance, high cholesterol, fatty liver, and a greater risk for diabetes, heart disease, and strokeare all related to obesity, but, according to a review in the March 9th issue of the Cell Press publication Trends in Endocrinology and Metabolism, not in the way you probably think they are.

In fact, says Roger Unger of the University of Texas Southwestern at Dallas, obesity is the body's way of storing lipids where they belong, in fat tissue, in an effort to protect our other organs from lipids' toxic effects. It's when the surplus of calories coming in gets to be too much for our fat tissue to handle that those lipids wind up in other places they shouldn't be, and the cascade of symptoms known as metabolic syndrome sets in.

It comes down to simple facts that all of us know on some level or another: Americans since the 1950s eat too much high-calorie food loaded with carbs and fat (what Unger calls "potent adipogenic nutrient mixtures") and, thanks to modern technology, we move far too little. Until that changes, Unger doesn't see any end to the growing epidemic of metabolic syndrome. Still, our metabolisms aren't broken; the pathways that squirrel fat away as an energy source for use in lean times are just completely overwhelmed. "We are pushing our homeostatic capability to the maximum," says Unger, who coined the term "lipotoxicity" in 1994. "Overnutrition used to be rarereserved for those in the castle. Today, it's just the opposite. Bad calories are so cheap that anyone can afford to get overweight."

Unger cites plenty of evidence in support of a protective role for obesity. Genetic manipulations in mice that increase or decrease fat formation have provided evidence that adipogenesis, meaning the generation of fat cells, delays other metabolic consequences of overeating. The reverse is also true, he writes. Obesity-resistant mice have in some cases been found to develop severe diabetes upon eating too much, as a result of lipid accumulation in tissues other than fat...

Mother's Milk Turns On The Heat

In newborn mice, at least, mother's milk appears to have some rather immediate and potentially far-reaching metabolic consequences. The milk intake kick-starts the liver to produce a molecule that then turns on heat-generating brown fat.

"A key phenomenon required after birth is to adapt the body to a lower environmental temperature with respect to that experienced when the fetus is inside the mother's womb," said Francesc Villarroya of the University of Barcelona. "We find that a key inducer of heat production in neonates is FGF21, released by the liver in response to the initiation of suckling."...

In Immune-Altered Mice Intestinal Bacteria Drive Obesity And Metabolic Disease

Increased appetite and insulin resistance can be transferred from one mouse to another via intestinal bacteria, according to research being published online this week by Sciencemagazine.

The finding strengthens the case that intestinal bacteria can contribute to human obesity and metabolic disease, since previous research has shown that intestinal bacterial populations differ between obese and lean humans.

Blood glucose-lowering hormone FGF21 also activates brown adipose tissue metabolism

The blood glucose-lowering hormone FGF21 is also an activator of brown adipose tissue metabolism, according to the study featured on the cover of Cell Metabolism and directed by the lecturer Francesc Villarroya of the UB's Department of Biochemistry and Molecular Biology (Faculty of Biology), the Institute of Biomedicine, and the Biomedical Research Networking Centre in Physiopathology of Obesity and Nutrition.

The study was carried out using newborn mice, and reveals possible new therapeutic targets for combating obesity using the fibroblast growth factor 21 (FGF21), which is secreted by the liver in response to fats in the diet. The team behind the research describe a novel action of FGF21 on brown adipose tissue, which governs energy expenditure and heat production in the body.

FGF21 is an antidiabetic and antiobesity agent that has been referred to in scientific literature since 2005", says Francesc Villarroya, an expert in the study of metabolism regulation models using genetically modified mice. He explains that, "Our study provides the first evidence that FGF21 causes thermogenesis in brown adipose tissue, that is, the burning of calories to release heat, dissipating large amounts of energy. Any agent that promotes and activates brown adipose tissue metabolism is, by definition, an antiobesity agent"...

Transgenic Mice Could Solve The Obesity Epidemic

By tweaking an enzyme in mice, researchers expected to get rodents with low cholesterol, but fatty livers. Instead they found a switch which might be a weight loss miracle.

The researchers from the University of Alberta bred a mouse lacking a single enzyme that's associated with fat metabolism — triacylglycerol hydrolase (TGH). TGH is partly responsible for releasing triglycerides from the liver where they go on to form very low-density lipoproteins (VLDLs), which are considered "bad" cholesterol. The scientists thought that breeding a mouse deficient in TGH would have fewer VLDLs, and instead found the mice that not only had lower cholesterol, but also system wide metabolic improvement — seemingly without downside.

The researchers hypothesized that removing the TGH would mean the more fat would build up in the liver, as the mechanism by which the fat was released was missing. Instead of getting tiny rodent foie gras, the triglycerides were burned almost immediately rather than being stored, and the liver compensated by synthesizing less fat. The rodents ate more, but also expended more energy, and showed no change in body weight compared to their normal cousins...

BPA And Obese Babies: Is There A Connection?

Drive-thru burgers and fries, movie theater popcorn with three days worth of fat and calories, video games, smart phones and TV, there are plenty of villains in the war against obesity. But all of the usual suspects don't explain the latest segment of the population with rising obesity rates – infants.

Research from Harvard University shows infant obesity has risen more than 70 percent since 1980. The numbers are staggering and confusing because babies eat only formula or breast milk and they've never been much into exercise.

"I get the question you know, 'how old is she?'. When I say 'six weeks', they say she looks like a three month old. She's definitely bigger," explained new mother Kelly Domina.

Domina is confident her 6-week old daughter will outgrow her baby fat but studies have shown big babies are at risk of being obese adults.

WHY ARE BABIES GETTING FAT?

Researchers believe a common household chemical may be to blame.

"Research has shown since 2001 that being exposed to BPA during development changes your body weight," explained Tufts University Scientist Dr. Laura Vandenberg.

BPA, or Bisphenol-A, is found in hundreds of consumer products. "Humans are most likely exposed to BPA through oral exposures," Vandenberg said. "BPA is used to line the inside of cans and that's thought to be a major exposure in adults."

Dr. Vandenberg and her colleagues have evidence that mice exposed to tiny amounts of BPA while in the womb gained more weight than mice that were not exposed. The animals didn't eat more and they got the same amount of exercise. "What actually happens is the fat cells have more fat in them so each cell is actually getting larger," Vandenberg said...

Soluble Rich-Fiber Foods Boost Immunity and Reduce Obesity, Study Reveals

A recent study at the University of Illinois has re-confirmed a very famous saying "An apple a day keeps doctor away" by concluding that soluble-fiber rich foods like oats, apples, and nuts not only help in lessening inflammation that leads to obesity, but also are capable of strengthening the immune system. It was found that the soluble fiber products produce interleukin-4, which is an anti-inflammatory protein.

Elaborating on the study, Gregory Freund, a Professor in the University of Illinois' College of Medicine said, "Soluble fiber changes the personality of immune cells, they go from being pro-inflammatory, angry cells to anti-inflammatory, healing cells that help us recover faster from infection".

In this study, laboratory mice were experimented as they were made to consume identical low-fat diets with soluble or insoluble fibers for six weeks. This study is expected to be published in the May 2010 issue of Brain, Behavior, and Immunity.

With Just One Enzyme Missing, Mice Show 'Global' Metabolic Improvements

When researchers created mice lacking an enzyme that breaks down and releases stored triglycerides (more properly known as triacylglycerols or TGs), they expected to see animals with better lipid profiles. But according to a report in the March Cell Metabolism, a Cell Press publication, they got more than they bargained for. The triacylglycerol hydrolase (TGH)-deficient mice showed global metabolic benefits, with essentially no downside.

"It was a surprising and unexpected finding," said Richard Lehner of the University of Alberta. "With this gene deleted, not only was there a decline in very low-density lipoproteins in the whole mouse, it also affected metabolism in fat tissue. The insulin-secreting cells became smaller, suggesting that they didn't have to work as hard to secrete insulin, and the mice became more insulin sensitive." The animals ate more, but they also expended more energy and showed no change in body weight.

Very low-density lipoproteins (VLDLs) are a form of "bad" cholesterol, Lehner explained. TGH normally frees up triglycerides from their storage place in the liver, releasing them for assembly into VLDLs. Therefore, one might expect that loss of TGH would have ill effects on the liver, as triglycerides would build up there. Indeed, he says, similar experiments with other enzymes have shown such an effect.

"We didn't observe that here," Lehner said. "Instead of being stored in liver, triglycerides were directed for oxidation." In other words, they were burned. The liver also compensated by synthesizing less fat.

The studies demonstrate the potential of TGH as a therapeutic target for lowering blood lipid levels, with possible far-reaching beneficial side effects throughout the body. That may be especially worthy of note, given that drug companies already have a TGH blocker. In fact, Lehner's team earlier showed that the TGH-inhibiting drug can lower the secretion of VLDLs from liver cells. But it wasn't clear whether the drug was really acting only on TGH. The new findings add support to the notion that loss of TGH activity alone can have very significant and positive effects...