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...
Sunday, October 31, 2010
Biochemical Approach to Treating Diabetes May Replace Diabetes Drugs
A surprise discovery of a protein that helps regulate glucose may be especially good news for shift workers, and could lead to new ways of treating obesity and diabetes.
Online PR News – 27-October-2010 – Biologists experimenting with mice have uncovered a possible new biological approach to treating obesity and type 2 diabetes. Their work also raises some interesting questions about the role disturbances in the human sleep cycle plays in the rise of diabetes in the US and other industrialized countries...
Online PR News – 27-October-2010 – Biologists experimenting with mice have uncovered a possible new biological approach to treating obesity and type 2 diabetes. Their work also raises some interesting questions about the role disturbances in the human sleep cycle plays in the rise of diabetes in the US and other industrialized countries...
OSU study links light exposure to obesity in mice
A recent Ohio State study found that eight weeks of exposure to light at night caused mice to gain nearly 50 percent more weight than mice given eight hours of darkness daily...
Sunday, October 24, 2010
Study says sitting down changes our body chemistry
If you're sitting down you may want to get up and take a walk around. A new study says that sitting actually changes our bed (sic) chemistry, affecting how long we live. Researchers found that when lab mice were prevented from running around they put on weight. Being sedentary turns off an important chemical that burns fat.
People sitting longer than six hours a day are more likely to die from diabetes, heart disease and obesity. Men are 18% more likely, women are 37%.
People sitting longer than six hours a day are more likely to die from diabetes, heart disease and obesity. Men are 18% more likely, women are 37%.
Gluttonous Male Mice Give Diabetes to Daughters
A prospective dad’s diet may affect the health of his future children, suggests a study of cross-generational nutritional impacts in mice.
Males were fed a high-fat diet, becoming obese and diabetic, then mated with lean, healthy females. At six weeks of age, or the mouse equivalent of puberty, their daughters became glucose-intolerant, a major step toward diabetes.
That overweight moms are more likely to have overweight babies is known, but the phenomenon hadn’t before been demonstrated in males of any species...
Males were fed a high-fat diet, becoming obese and diabetic, then mated with lean, healthy females. At six weeks of age, or the mouse equivalent of puberty, their daughters became glucose-intolerant, a major step toward diabetes.
That overweight moms are more likely to have overweight babies is known, but the phenomenon hadn’t before been demonstrated in males of any species...
Shining a Night Light on Obesity
f you're wishing upon a star in hopes to stop packing on the pounds, you might already be jinxing yourself. A recent study finds that continual exposure to light at night may lead to weight gain, even without changing physical activity or eating more food. Researchers say that instead of wishing upon the stars . . . maybe you should sleep under them.
Researchers found that mice that were exposed to a moderately dim light at night over eight weeks had a body mass that was around 50 percent more than other mice that lived in a standard light-dark cycle. "Although there were no differences in activity levels or daily consumption of food, the mice that lived with light at night were getting fatter than the others," which Laura Fonken, lead author of the study and a doctoral student in neuroscience at Ohio State University, was quoted as saying.
The study revealed that the mice living with light at night eat at times they normally wouldn't, which is a main factor of their weight gain. One study showed that mice exposed to light at night -- but with food restricted to normal eating times -- gained no more weight than did mice in a normal light-dark cycle.
"Something about light at night was making the mice in our study want to eat at the wrong times to properly metabolize their food," which Randy Nelson, co-author of the study and professor of neuroscience and psychology at Ohio State, was quoted as saying. If these results are confirmed in humans, it would verify that late-night snacking is a possible risk factor for obesity.
In another study, mice were housed in one of three condition: 24 hours of constant light, a standard light-dark cycle (16 hours of light at 150 lux, 8 hours of dark), or 16 hours of daylight and 8 hours of dim light (approximately 5 lux of light).
Researchers measured the amount of food the mice ate each day, in addition to how much they moved in their cages each day using an infrared beam crossing system. Furthermore, body mass was calculated each week. Compared to mice in the standard dark-light cycle, mice that were exposed to dim light at night showed notably higher increases in body mass, beginning in the commencement of the study and continuing to end.
Light-at-night mice had gained 12 grams of body mass by the end of the experiment, compared to 8 grams for those in the standard light-dark cycle. It was reported that mice in constant bright light additionally gained more than those in the standard light-dark cycle; however the scientists stated that the dim light-at-night mice were better comparisons to the light exposure human generally are exposed to.
What's more, the dim light-at-night mice showed higher levels of epididymal fat as well as impaired glucose tolerance - a marker for pre-diabetes...
Researchers found that mice that were exposed to a moderately dim light at night over eight weeks had a body mass that was around 50 percent more than other mice that lived in a standard light-dark cycle. "Although there were no differences in activity levels or daily consumption of food, the mice that lived with light at night were getting fatter than the others," which Laura Fonken, lead author of the study and a doctoral student in neuroscience at Ohio State University, was quoted as saying.
The study revealed that the mice living with light at night eat at times they normally wouldn't, which is a main factor of their weight gain. One study showed that mice exposed to light at night -- but with food restricted to normal eating times -- gained no more weight than did mice in a normal light-dark cycle.
"Something about light at night was making the mice in our study want to eat at the wrong times to properly metabolize their food," which Randy Nelson, co-author of the study and professor of neuroscience and psychology at Ohio State, was quoted as saying. If these results are confirmed in humans, it would verify that late-night snacking is a possible risk factor for obesity.
In another study, mice were housed in one of three condition: 24 hours of constant light, a standard light-dark cycle (16 hours of light at 150 lux, 8 hours of dark), or 16 hours of daylight and 8 hours of dim light (approximately 5 lux of light).
Researchers measured the amount of food the mice ate each day, in addition to how much they moved in their cages each day using an infrared beam crossing system. Furthermore, body mass was calculated each week. Compared to mice in the standard dark-light cycle, mice that were exposed to dim light at night showed notably higher increases in body mass, beginning in the commencement of the study and continuing to end.
Light-at-night mice had gained 12 grams of body mass by the end of the experiment, compared to 8 grams for those in the standard light-dark cycle. It was reported that mice in constant bright light additionally gained more than those in the standard light-dark cycle; however the scientists stated that the dim light-at-night mice were better comparisons to the light exposure human generally are exposed to.
What's more, the dim light-at-night mice showed higher levels of epididymal fat as well as impaired glucose tolerance - a marker for pre-diabetes...
Tuesday, October 19, 2010
Obesity therapy gains as test rats don’t overeat
One of the more offbeat ideas in the business of developing drugs to treat obesity has some new evidence behind it.
Boston-based Gelesis, the developer of a super-absorbent capsule designed to swell up in the stomach and make people feel full, said its treatment was able to help rats reduce their food intake over 18 hours. The findings were presented at the Obesity Society’s recent annual meeting in San Diego.
While it’s too early to say the treatment will work in people, many other weight-loss drugs have been tripped up by safety concerns. But the rat study is interesting, in part, because it comes about six months after Gelesis reported on a more rigorous clinical trial of 95 patients. The other study showed that the capsules helped people feel full after meals and less hungry in between...
Boston-based Gelesis, the developer of a super-absorbent capsule designed to swell up in the stomach and make people feel full, said its treatment was able to help rats reduce their food intake over 18 hours. The findings were presented at the Obesity Society’s recent annual meeting in San Diego.
While it’s too early to say the treatment will work in people, many other weight-loss drugs have been tripped up by safety concerns. But the rat study is interesting, in part, because it comes about six months after Gelesis reported on a more rigorous clinical trial of 95 patients. The other study showed that the capsules helped people feel full after meals and less hungry in between...
Sunday, October 17, 2010
Phospholipid shows anti-obesity potential, in mice at least
Supplementation of the diet with the phospholipid phosphatidylinositol may exert an anti-obesity effect by modifying gene expression in the liver, suggests a new study with mice.
If the findings, published in the Journal of Agricultural and Food Chemistry, can be repeated in further studies, it could see phosphatidylinositol established as an ingredient with potential weight management potential...
If the findings, published in the Journal of Agricultural and Food Chemistry, can be repeated in further studies, it could see phosphatidylinositol established as an ingredient with potential weight management potential...
Nighttime Light Ups Weight in Mice
The gentle glow of the television at night may be contributing to the obesity epidemic, findings from a mouse study suggest.
Mice exposed to even dim light at night gained significantly more weight and lost glucose tolerance compared with mice housed in a dark environment at night, Laura K. Fonken, a graduate student at Ohio State University, in Columbus, and colleagues found.
The night light-exposed mice didn't eat more or move around less overall, but did shift to more munching at off hours when they were inactive...
Mice exposed to even dim light at night gained significantly more weight and lost glucose tolerance compared with mice housed in a dark environment at night, Laura K. Fonken, a graduate student at Ohio State University, in Columbus, and colleagues found.
The night light-exposed mice didn't eat more or move around less overall, but did shift to more munching at off hours when they were inactive...
Sunday, October 10, 2010
Getting to the bottom of diabetes and kidney disease
Diabetic kidney disease may result as much from a failure of certain renal cells to access insulin as it does from runaway blood sugar, a new study shows. The findings in mice suggests that targeting the condition known as insulin resistance might protect the kidneys of people with diabetes, researchers report in the October Cell Metabolism.
Fully half of all kidney disease that leads to dialysis or a transplant occurs in people with diabetes, and most have the common type 2 form that typically shows up in adulthood. Type 2 diabetes has clear links to obesity, lack of exercise and insulin resistance in which cells fail to capture glucose efficiently from the bloodstream after digestion of food. While the precise cause of insulin resistance remains unclear, there’s no question it starves cells, forces the pancreas to work overtime making more insulin and leaves a person with high blood sugar...
Fully half of all kidney disease that leads to dialysis or a transplant occurs in people with diabetes, and most have the common type 2 form that typically shows up in adulthood. Type 2 diabetes has clear links to obesity, lack of exercise and insulin resistance in which cells fail to capture glucose efficiently from the bloodstream after digestion of food. While the precise cause of insulin resistance remains unclear, there’s no question it starves cells, forces the pancreas to work overtime making more insulin and leaves a person with high blood sugar...
Video feature: Developing a treatment for obesity based on natural appetite suppression
Over 30 000 deaths a year are caused by obesity in England alone and yet the need for safe and effective anti-obesity therapies is largely unmet. With funding from the Wellcome Trust's Seeding Drug Discovery initiative in 2007, Professor Bloom and his team have developed a novel, synthetic form of pancreatic polypeptide that can cause a significant reduction in food intake and body weight in mice. The lead compound, PP1420, entered phase I clinical trials in mid2010. If successful, the proposed research may lead to a treatment within five - eight years.
Saturday, October 02, 2010
Blueberries Help Fight Artery Hardening, Lab Animal Study Indicates
Blueberries may help fight atherosclerosis, also known as hardening of the arteries, according to results of a preliminary U.S. Department of Agriculture (USDA)-funded study with laboratory mice. The research provides the first direct evidence that blueberries can help prevent harmful plaques or lesions, symptomatic of atherosclerosis, from increasing in size in arteries...
Sunday, September 26, 2010
Enzyme blocker keeps mice slim
Blocking a single brain enzyme helped short-circuit a key hunger signal in mice and made them eat less, lose weight and have better blood sugar control, U.S. researchers said on Tuesday.
While much more research lies ahead, they said the finding may lead to new treatments for obesity and diabetes in humans.
"We believe we have identified an important drug development target that could potentially turn into a metabolic triple play: appetite control, weight loss and blood sugar management," said Tony Means of Duke University Medical Center in Durham, North Carolina, whose study appears in the journal Cell Metabolism.
Dr. Means's team focused on the enzyme CaMKK2, which plays a role in appetite stimulation in mice and in humans. Found in a region of the brain known as the hypothalamus, it takes its orders from a hormone released in the gut known as ghrelin, which is released when the stomach is empty.
Ghrelin is already linked to appetite control.
In a separate brain imaging study in the same journal, researchers at the Neurological Institute at McGill University in Montreal showed that ghrelin not only makes people feel hungry, but it makes food look more appealing by activating pleasure signals in the brain.
Dr. Means's idea is to find a way to interrupt ghrelin's activity by toning down the CaMKK2 enzyme's response to the hunger signal.
His team found that mice genetically engineered to lack the enzyme CaMKK2 stayed slim regardless of whether they were on a low-fat or high-fat diet...
While much more research lies ahead, they said the finding may lead to new treatments for obesity and diabetes in humans.
"We believe we have identified an important drug development target that could potentially turn into a metabolic triple play: appetite control, weight loss and blood sugar management," said Tony Means of Duke University Medical Center in Durham, North Carolina, whose study appears in the journal Cell Metabolism.
Dr. Means's team focused on the enzyme CaMKK2, which plays a role in appetite stimulation in mice and in humans. Found in a region of the brain known as the hypothalamus, it takes its orders from a hormone released in the gut known as ghrelin, which is released when the stomach is empty.
Ghrelin is already linked to appetite control.
In a separate brain imaging study in the same journal, researchers at the Neurological Institute at McGill University in Montreal showed that ghrelin not only makes people feel hungry, but it makes food look more appealing by activating pleasure signals in the brain.
Dr. Means's idea is to find a way to interrupt ghrelin's activity by toning down the CaMKK2 enzyme's response to the hunger signal.
His team found that mice genetically engineered to lack the enzyme CaMKK2 stayed slim regardless of whether they were on a low-fat or high-fat diet...
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