A fat yet muscular mouse is helping researchers learn whether more muscle improves the cardiovascular health of obese individuals.
"We are looking for ways to counteract the unhealthy effects of fat," said Dr. David Stepp, vascular biologist at the Medical College of Georgia Vascular Biology Center and co-director of MCG's Diabetes & Obesity Discovery Institute.
Obesity increases the risk for cardiovascular disease as well as diabetes, which essentially doubles the cardiovascular risk. But Stepp's laboratory research indicates more muscle could reduce that risk - a theory bolstered by people who appear "fit and fat." He recently received a $450,000 exploratory grant from the National Institutes of Health to further explore the possibilities.
The fact is that people - and mice - with more muscle have more blood vessels, use more oxygen and energy and eliminate more glucose even sitting still than their flabbier counterparts. "Fat does not consume a lot of energy and it's not very vascular," Stepp said. "Muscle and nerves, on the other hand, generate electricity, which is one of the most energetically expensive things we do." The heart and blood vessels also thrive with increased blood flow and diabetes risk is reduced by muscles' glucose disposal capabilities...
Sunday, November 28, 2010
The fat cat cometh
IN THEIR attempts to explain the global epidemic of obesity, researchers have often taken to fingering culprits beyond people’s direct control. It is now believed that increased levels of stress, climate change and even artificial light at night may contribute to expanding waistlines. However, if such factors affect humans, they ought, in principle, to have similarly nefarious effects on other creatures. This should hold especially true for species that are physiologically similar to people and live in proximity to them. Pet owners have long fretted that this may, indeed, be happening.
Of course, anecdotal evidence carries little weight, so a group of researchers led by Yann Klimentidis, of the University of Alabama, decided to check whether animal obesity rates do in fact mirror the worrying trend among people. They published their findings this week in the Proceedings of the Royal Society.
Dr Klimentidis and his team set about their task by scouring online repositories of scientific papers, contacting fellow researchers and even petitioning pet-food companies for data on changes in animals’ bodyweights over the decades. They limited their search to mammals, whose bodies work much like humans’ do—and, specifically, to those mammals living with or around people in the rich world.
The trawl threw up information on more than 20,000 animals from 24 distinct populations covering eight species. These included cats, dogs, mice, rats and several types of monkey. Some were bred in highly controlled research environments. Others lived in people’s homes or in the wild. None had their food intake artificially limited or, as with livestock, ramped up...
Of course, anecdotal evidence carries little weight, so a group of researchers led by Yann Klimentidis, of the University of Alabama, decided to check whether animal obesity rates do in fact mirror the worrying trend among people. They published their findings this week in the Proceedings of the Royal Society.
Dr Klimentidis and his team set about their task by scouring online repositories of scientific papers, contacting fellow researchers and even petitioning pet-food companies for data on changes in animals’ bodyweights over the decades. They limited their search to mammals, whose bodies work much like humans’ do—and, specifically, to those mammals living with or around people in the rich world.
The trawl threw up information on more than 20,000 animals from 24 distinct populations covering eight species. These included cats, dogs, mice, rats and several types of monkey. Some were bred in highly controlled research environments. Others lived in people’s homes or in the wild. None had their food intake artificially limited or, as with livestock, ramped up...
http://www.bionews.org.uk/page_82515.asp
Scientists have found a direct link between the 'fat mass and obesity associated' (Fto) gene and increased weight. Research published in 2007 uncovered an association between variations in the Fto gene and increased body weight in humans.
The Fto gene is not the only gene associated with increased predisposition to obesity, but it is the most significant genetic factor so far identified. Seventeen percent of Europeans have two copies of a common Fto variant. On average, this population is 3kg heavier and has a 1.3 times greater likelihood of being obese.
Until now it was not known whether the link between obesity and Fto was direct or caused by some other factor. The team at MRC Harwell in Oxford predicted that increased expression of Fto may be causing obesity since the Fto variant in humans has been linked to increased expression of the gene in some tissues. To test this, they bred mice with extra copies of the Fto gene.
The team found that the test mice became fatter than the normal mice. What's more, the increase in weight gain was greater the more copies of the gene the test mice had. The researchers attributed the weight gain to an increase in food intake rather than differences in the way the mice metabolise their food...
The Fto gene is not the only gene associated with increased predisposition to obesity, but it is the most significant genetic factor so far identified. Seventeen percent of Europeans have two copies of a common Fto variant. On average, this population is 3kg heavier and has a 1.3 times greater likelihood of being obese.
Until now it was not known whether the link between obesity and Fto was direct or caused by some other factor. The team at MRC Harwell in Oxford predicted that increased expression of Fto may be causing obesity since the Fto variant in humans has been linked to increased expression of the gene in some tissues. To test this, they bred mice with extra copies of the Fto gene.
The team found that the test mice became fatter than the normal mice. What's more, the increase in weight gain was greater the more copies of the gene the test mice had. The researchers attributed the weight gain to an increase in food intake rather than differences in the way the mice metabolise their food...
Sunday, November 21, 2010
Genes 'regulating obesity' in men found
Scientists have found genes that contribute to the risk of obesity in men.
A genome-wide linkage scan for high body mass index (BMI) in 3,893 men and 4,445 women has identified a link on chromosome 5q13-15.
Analysis of this chromosome has revealed a rare cluster of gene types linked to high BMI in men but not women. The portion of the chromosome related to high BMI risk contains a single gene named "arrestin domain containing 3" (Arrdc3).
Researchers investigated Arrdc3 expression and detected it in human fat and muscle. Analysis of gene expression in human abdominal fat biopsies showed significant correlation of Arrdc3 messenger RNA with BMI in men but not women, supporting the male-specific linkage to obesity.
The study also found that fasting increased Arrdc3 expression in both human and mouse fat tissue, suggesting that Arrdc3 functions to conserve energy when food is not available.
To test whether the gene causally regulates obesity, the scientist generated a mouse without Arrdc3. The mice without Arrdc3 showed a "striking resistance" to age-induced obesity: ale mice without Arrdc3 had a smaller total body mass compared to mice with the gene...
A genome-wide linkage scan for high body mass index (BMI) in 3,893 men and 4,445 women has identified a link on chromosome 5q13-15.
Analysis of this chromosome has revealed a rare cluster of gene types linked to high BMI in men but not women. The portion of the chromosome related to high BMI risk contains a single gene named "arrestin domain containing 3" (Arrdc3).
Researchers investigated Arrdc3 expression and detected it in human fat and muscle. Analysis of gene expression in human abdominal fat biopsies showed significant correlation of Arrdc3 messenger RNA with BMI in men but not women, supporting the male-specific linkage to obesity.
The study also found that fasting increased Arrdc3 expression in both human and mouse fat tissue, suggesting that Arrdc3 functions to conserve energy when food is not available.
To test whether the gene causally regulates obesity, the scientist generated a mouse without Arrdc3. The mice without Arrdc3 showed a "striking resistance" to age-induced obesity: ale mice without Arrdc3 had a smaller total body mass compared to mice with the gene...
'Hunger hormone' activating enzyme holds promise as obesity target
Blocking a key gut enzyme involved in the hunger response can reduce weight gain in mice, say US and Taiwanese researchers. The approach could eventually lead to treatments for obesity in humans that would work by damping down hunger pangs.
The market for obesity drugs is worth over $1 billion (£625 million) a year, with some 300 million potential patients. A current focus for drug developers is synthetic hormones that mimic the actions of gut hormones involved in controlling blood sugar levels. Some have already been approved for use in diabetes...
The market for obesity drugs is worth over $1 billion (£625 million) a year, with some 300 million potential patients. A current focus for drug developers is synthetic hormones that mimic the actions of gut hormones involved in controlling blood sugar levels. Some have already been approved for use in diabetes...
'Fat gene' may lead to a thin pill
...People with two copies of the genetic variant – about 16 per cent of all Europeans – were on average 3kg (6.6lbs) heavier than those without it.
In this latest study, scientists bred mice with extra copies of the FTO gene. They found that the test mice, although healthy, ate more and became fatter than normal mice.
Prof Frances Ashcroft, one of the leaders of the research, said: "This work makes us confident that FTO is an important gene that contributes to obesity.
"We can now think about developing drugs that turn down the activity of the FTO gene as potential anti-obesity pills. That's a long way off and there's no certainty of success, but it's an enticing prospect."...
In this latest study, scientists bred mice with extra copies of the FTO gene. They found that the test mice, although healthy, ate more and became fatter than normal mice.
Prof Frances Ashcroft, one of the leaders of the research, said: "This work makes us confident that FTO is an important gene that contributes to obesity.
"We can now think about developing drugs that turn down the activity of the FTO gene as potential anti-obesity pills. That's a long way off and there's no certainty of success, but it's an enticing prospect."...
Monday, November 08, 2010
Born to be fat
...Studies on animals have shown that exposure around the time of birth to even trace amounts of everyday chemicals can predispose subjects to weight gain throughout life. Perfluorooctanoic acid, found in non-stick pans, microwave popcorn bags and pizza boxes, has been associated with obesity in female mice. Bisphenol A, used in plastics and recently declared a toxic chemical in Canada, is linked to obesity in rats. Similarly, triclosan, an ingredient in antibacterial hand soaps, dishwashing detergents and other body care products, has been correlated to faster growth in frogs. Caren Helbing, a researcher at the University of Victoria who worked on the triclosan study, notes, “It’s critical to realize that some of the manufactured chemicals that have been important for protecting people, like flame retardants, were designed without thinking about how they would change the way hormones in humans work.”
The grandfather of the obesogen studies is Bruce Blumberg, a cell biologist at the University of California, Irvine. He coined the term “obesogen,” and has focused on mice and how they are affected by tributyltin (TBT), a pesticide added to paint used on ships to prevent the growth of marine organisms like barnacles and algae, which enters underwater environments and ends up in our seafood. “We found that if we treat pregnant mice with tributyltin, the pups in their womb will be predisposed to getting fat later in life,” Blumberg says. “They make more fat cells, and that appears to lead them to be heavier.”..
The grandfather of the obesogen studies is Bruce Blumberg, a cell biologist at the University of California, Irvine. He coined the term “obesogen,” and has focused on mice and how they are affected by tributyltin (TBT), a pesticide added to paint used on ships to prevent the growth of marine organisms like barnacles and algae, which enters underwater environments and ends up in our seafood. “We found that if we treat pregnant mice with tributyltin, the pups in their womb will be predisposed to getting fat later in life,” Blumberg says. “They make more fat cells, and that appears to lead them to be heavier.”..
Saturday, November 06, 2010
Gastric Bypass Alters Sweet Taste Function
Gastric bypass surgery decreases the preference for sweet-tasting substances in obese rats, a study finding that could help in developing safer treatments for the morbidly obese, according to Penn State College of Medicine researchers.
"Roux-en-Y gastric bypass surgery is the most common effective treatment for morbid obesity," said Andras Hajnal, M.D., Ph.D., associate professor, Department of Neural and Behavioral Science and Surgery. "Many patients report altered taste preferences after having the procedure."
This surgery involves the creation of a small gastric pouch and bypassing a portion of the upper small intestine. Unlike other weight-reduction methods, it produces substantial and durable weight loss and significant improvements in obesity-related medical conditions including diabetes.
Study results in obese rats suggest that post-surgery changes in the gastrointestinal anatomy affect change in the brain that relate to taste...
"Roux-en-Y gastric bypass surgery is the most common effective treatment for morbid obesity," said Andras Hajnal, M.D., Ph.D., associate professor, Department of Neural and Behavioral Science and Surgery. "Many patients report altered taste preferences after having the procedure."
This surgery involves the creation of a small gastric pouch and bypassing a portion of the upper small intestine. Unlike other weight-reduction methods, it produces substantial and durable weight loss and significant improvements in obesity-related medical conditions including diabetes.
Study results in obese rats suggest that post-surgery changes in the gastrointestinal anatomy affect change in the brain that relate to taste...
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