...Unlike mice fed a typical low-fat laboratory diet, adjusting their intake to the ambient temperature, mice fed high-fat diets do not decrease their food intake at higher temperatures and gain weight.
"These human and animal experimental models suggest that while intake is somewhat suppressed at higher temperatures, this is unlikely to fully compensate for the reduced energy expenditure of a warm environment particularly where highly palatable foods are available," Johnson and colleagues observed.
This research argues in favor of a causal link between increased time spent in thermal comfort and weight gain in the population, they said...
Sunday, January 30, 2011
Obesity Drug Moving to Clinical Trials Following Success in Mice, Dogs, and Women
A successful trial on a small number of obese women in Australia demonstrated that those treated with intravenous Zafgen-433 lost an average of approximately two pounds per week. In addition to the weight loss, the women experienced a decline in hunger and reductions in triglycerides and low-density lipoprotein (LDL) cholesterol levels, all with no serious, treatment-related adverse events. Now, following the positive results of this initial double-blind, placebo-controlled, proof-of-concept trial, Zafgen expects to have a subcutaneous form of the drug ready by the end of summer which will be used for the next phase of clinical trials (for both men and women) expected to begin sometime later in 2011. Ultimately, though, the company plans to create a conventional, oral form of the medication...
Zafgen's innovative approach to reversing obesity targets adipose tissue (fat cells) because, unlike the traditional view of obesity that fat accumulation is a "passive result of other factors," Zafgen views adipose tissue "as playing an active role in the disease," a view that represents a "fundamentally new paradigm" in how obesity is regarded and potentially treated. Indeed, obese people release fat from their adipose tissue at a slower rate than the non-obese, and they convert it to ketone bodies – a form that is usable as fuel for muscles – at a slower rate. (Much of this process encompasses the metabolic syndrome and insulin resistance that doctors described when discussing obesity as a risk for type 2 diabetes.) Zafgen-433 acts on adipose tissue by inhibiting an enzyme called methionine aminopeptidase 2, or MetAP2, an enzyme that is associated with the body's tendency for preserving its stores of fat. When this enzyme is inhibited by the drug, it allows the body to metabolize fatty acids at a more normalized rate as the body re-establishes its balance, leading to a substantial loss of body weight in overweight individuals. This was true for the overfed mice (pictured above), for overweight dogs, and for the initial trial of obese women in Australia. Adipose tissue samples from the treated mice revealed that their fat cells actually shrank...
Zafgen's innovative approach to reversing obesity targets adipose tissue (fat cells) because, unlike the traditional view of obesity that fat accumulation is a "passive result of other factors," Zafgen views adipose tissue "as playing an active role in the disease," a view that represents a "fundamentally new paradigm" in how obesity is regarded and potentially treated. Indeed, obese people release fat from their adipose tissue at a slower rate than the non-obese, and they convert it to ketone bodies – a form that is usable as fuel for muscles – at a slower rate. (Much of this process encompasses the metabolic syndrome and insulin resistance that doctors described when discussing obesity as a risk for type 2 diabetes.) Zafgen-433 acts on adipose tissue by inhibiting an enzyme called methionine aminopeptidase 2, or MetAP2, an enzyme that is associated with the body's tendency for preserving its stores of fat. When this enzyme is inhibited by the drug, it allows the body to metabolize fatty acids at a more normalized rate as the body re-establishes its balance, leading to a substantial loss of body weight in overweight individuals. This was true for the overfed mice (pictured above), for overweight dogs, and for the initial trial of obese women in Australia. Adipose tissue samples from the treated mice revealed that their fat cells actually shrank...
Sunday, January 23, 2011
Effects of diet-induced obesity and voluntary wheel running on the microstructure of the murine distal femur
Backgound: Obesity and osteoporosis, two possibly related conditions, are rapidly expanding health concerns in modern society. Both of them are associated with sedentary life style and nutrition.
To investigate the effects of diet-induced obesity and voluntary physical activity we used high resolution micro-computed tomography (uCT) together with peripheral quantitative computed tomography (pQCT) to examine the microstructure of the distal femoral metaphysis in mice.
Methods: Forty 7-week-old male C57BL/6J mice were assigned to 4 groups: control (C), control + running (CR), high-fat diet (HF), and high-fat diet + running (HFR). After a 21-week intervention, all the mice were sacrificed and the left femur dissected for pQCT and uCT measurements.
Results: The mice fed the high-fat diet showed a significant weight gain (over 70% for HF and 60% for HFR), with increased epididymal fat pad mass and impaired insulin sensitivity.
These obese mice had significantly higher trabecular connectivity density, volume, number, thickness, area and mass, and smaller trabecular separation. At the whole bone level, they had larger bone circumference and cross-sectional area and higher density-weighted maximal, minimal, and polar moments of inertia.
Voluntary wheel running decreased all the cortical bone parameters, but increased the trabecular mineral density, and decreased the pattern factor and structure model index towards a more plate-like structure.
Conclusions: The results suggest that in mice the femur adapts to obesity by improving bone strength both at the whole bone and micro-structural level. Adaptation to running exercise manifests itself in increased trabecular density and improved 3D structure, but in a limited overall bone growth...
To investigate the effects of diet-induced obesity and voluntary physical activity we used high resolution micro-computed tomography (uCT) together with peripheral quantitative computed tomography (pQCT) to examine the microstructure of the distal femoral metaphysis in mice.
Methods: Forty 7-week-old male C57BL/6J mice were assigned to 4 groups: control (C), control + running (CR), high-fat diet (HF), and high-fat diet + running (HFR). After a 21-week intervention, all the mice were sacrificed and the left femur dissected for pQCT and uCT measurements.
Results: The mice fed the high-fat diet showed a significant weight gain (over 70% for HF and 60% for HFR), with increased epididymal fat pad mass and impaired insulin sensitivity.
These obese mice had significantly higher trabecular connectivity density, volume, number, thickness, area and mass, and smaller trabecular separation. At the whole bone level, they had larger bone circumference and cross-sectional area and higher density-weighted maximal, minimal, and polar moments of inertia.
Voluntary wheel running decreased all the cortical bone parameters, but increased the trabecular mineral density, and decreased the pattern factor and structure model index towards a more plate-like structure.
Conclusions: The results suggest that in mice the femur adapts to obesity by improving bone strength both at the whole bone and micro-structural level. Adaptation to running exercise manifests itself in increased trabecular density and improved 3D structure, but in a limited overall bone growth...
The Microbes In Our Gut Regulate Genes That Control Obesity And Inflammation
If you are looking to lose weight in the coming year, you may need help from an unexpected place: the bacteria in your gut. That's because scientists have discovered that the bacteria living in your intestines may play a far more significant role in weight loss and gastrointestinal problems than ever imagined. In a new research report published online in The FASEB Journal (http://www.fasebj.org), researchers show that a deficiency of Toll-like receptor 2 (Tlr2) - used by mammals (including humans) to recognize resident microbes in the intestines - leads to changes in gut bacteria that resemble those of lean animals and humans. This discovery builds on previous research demonstrating that a deficiency of TLR2 protects against obesity, while at the same time promoting gastrointestinal problems like excessive inflammation. It also shows that genes controlling TLR2 expression play a very important role in one's gastrointestinal health and weight management.
"Our work highlights the remarkable capacity for an orchestrated reprogramming of the intestinal inflammatory network to overcome significant genetic challenges in the mammalian bowel," said Richard Kellermayer, Ph.D., a researcher involved in the work from the Section of Pediatric Gastroenterology, Hepatology and Nutrition at Baylor College of Medicine in Houston. "The appropriate exploitation of this remarkable capacity may provide means for the prevention and optimized treatment of common metabolic (such as obesity and diabetes) and gastrointestinal disorders."
To make this discovery, Kellermayer and colleagues studied normal mice and mice deficient in TLR2 using the large intestinal lining of these mice. They compared the TLR2-deficient ones to the normal group, as well as the bacteria, the epigenome (more specifically DNA methylation, a molecular change in the DNA associated with decreased gene expression), and the gene expression of the animals. The researchers found that the absence of TLR2 leads to microbial changes in the gut that resemble lean animals and humans, as well as immunologic changes similar to those observed in ulcerative colitis...
"Our work highlights the remarkable capacity for an orchestrated reprogramming of the intestinal inflammatory network to overcome significant genetic challenges in the mammalian bowel," said Richard Kellermayer, Ph.D., a researcher involved in the work from the Section of Pediatric Gastroenterology, Hepatology and Nutrition at Baylor College of Medicine in Houston. "The appropriate exploitation of this remarkable capacity may provide means for the prevention and optimized treatment of common metabolic (such as obesity and diabetes) and gastrointestinal disorders."
To make this discovery, Kellermayer and colleagues studied normal mice and mice deficient in TLR2 using the large intestinal lining of these mice. They compared the TLR2-deficient ones to the normal group, as well as the bacteria, the epigenome (more specifically DNA methylation, a molecular change in the DNA associated with decreased gene expression), and the gene expression of the animals. The researchers found that the absence of TLR2 leads to microbial changes in the gut that resemble lean animals and humans, as well as immunologic changes similar to those observed in ulcerative colitis...
Sunday, January 16, 2011
A magic calorie ride
Bob, an office supervisor in Toronto, considers himself an addict. But the substance he’s prone to abusing isn’t drugs or alcohol—it’s food. “I would gorge on Raisinets, pizza, anything that I could get in quantity,” says Bob, 60, who asked that his last name not be used. He ran up a $4,000 Visa bill, almost all of it on food. Eating as a stress release, “I averaged about 15,000 calories a day.” He weighed 336 lb. at his heaviest. “I’m no scientist, but I think it’s an addiction,” he says. “When I read about how a drug addict behaves, my response is the same to food.”
The term “food addiction” is controversial, but recent studies have shown that high-calorie foods engage the same regions of the brain as drugs like heroin and cocaine. Over time, scientists say, a high-fat diet can impair the brain’s pleasure centres like those drugs do, encouraging ever-larger binges and making it harder to quit. Remarkably, a mother’s diet might even hard-wire her baby for obesity later on in life. “It’s too early to call it food addiction,” says Teresa Reyes of the University of Pennsylvania School of Medicine, who studies how the brain adapts to changes in diet. “But there is absolutely increasing evidence showing that the brain responds to high-sucrose, high-fat diets in a very similar way that it responds to drugs of abuse.”
At the Society for Neuroscience’s annual conference in November, Reyes presented her latest work: mice that were fed a high-fat diet for a long period of time, she found, showed changes in parts of their brains associated with pleasure and reward. Just like cocaine or heroin, unhealthy foods seem to trigger the brain’s pleasure centres, eventually desensitizing them. It becomes a vicious cycle. “To reach the same level of reward, the person needs to eat more rewarding food,” Reyes says. “It’s very similar to what happens in chronic drug abuse.” (This data is now under review before publication.)...
The term “food addiction” is controversial, but recent studies have shown that high-calorie foods engage the same regions of the brain as drugs like heroin and cocaine. Over time, scientists say, a high-fat diet can impair the brain’s pleasure centres like those drugs do, encouraging ever-larger binges and making it harder to quit. Remarkably, a mother’s diet might even hard-wire her baby for obesity later on in life. “It’s too early to call it food addiction,” says Teresa Reyes of the University of Pennsylvania School of Medicine, who studies how the brain adapts to changes in diet. “But there is absolutely increasing evidence showing that the brain responds to high-sucrose, high-fat diets in a very similar way that it responds to drugs of abuse.”
At the Society for Neuroscience’s annual conference in November, Reyes presented her latest work: mice that were fed a high-fat diet for a long period of time, she found, showed changes in parts of their brains associated with pleasure and reward. Just like cocaine or heroin, unhealthy foods seem to trigger the brain’s pleasure centres, eventually desensitizing them. It becomes a vicious cycle. “To reach the same level of reward, the person needs to eat more rewarding food,” Reyes says. “It’s very similar to what happens in chronic drug abuse.” (This data is now under review before publication.)...
Bacteria in the gut help control obesity and inflammation
Researchers at Baylor College of Medicine in Houston have discovered that the bacteria living in the intestines may play a far more significant role in weight loss and gastrointestinal problems than ever imagined.
They show that a deficiency of Toll-like receptor 2 (Tlr2)-used by mammals (including humans) to recognize resident microbes in the intestines-leads to changes in gut bacteria that resemble those of lean animals and humans.
This discovery builds on previous research demonstrating that a deficiency of TLR2 protects against obesity, while at the same time promoting gastrointestinal problems like excessive inflammation.
It also shows that genes controlling TLR2 expression play a very important role in one's gastrointestinal health and weight management.
The team studied normal mice and mice deficient in TLR2 using the large intestinal lining of these mice. They compared the TLR2-deficient ones to the normal group, as well as the bacteria, the epigenome and the gene expression of the animals.
The researchers found that the absence of TLR2 leads to microbial changes in the gut that resemble lean animals and humans, as well as immunologic changes similar to those observed in ulcerative colitis...
They show that a deficiency of Toll-like receptor 2 (Tlr2)-used by mammals (including humans) to recognize resident microbes in the intestines-leads to changes in gut bacteria that resemble those of lean animals and humans.
This discovery builds on previous research demonstrating that a deficiency of TLR2 protects against obesity, while at the same time promoting gastrointestinal problems like excessive inflammation.
It also shows that genes controlling TLR2 expression play a very important role in one's gastrointestinal health and weight management.
The team studied normal mice and mice deficient in TLR2 using the large intestinal lining of these mice. They compared the TLR2-deficient ones to the normal group, as well as the bacteria, the epigenome and the gene expression of the animals.
The researchers found that the absence of TLR2 leads to microbial changes in the gut that resemble lean animals and humans, as well as immunologic changes similar to those observed in ulcerative colitis...
New findings may lead to a novel treatment for obesity
Scientists have added a new twist to the body of evidence suggesting human obesity is due in part to genetic factors.
While studying hormone receptors in laboratory mice, researchers at Mayo Clinic's campus in Florida and Washington University School of Medicine identified a new molecular player responsible for the regulation of appetite and metabolism.
The authors report that mice engineered not to express the lipoprotein receptor LRP1, in the brain's hypothalamus, began to eat uncontrollably, growing obese as well as lethargic. They found that LRP1, a major transporter of lipids and proteins into brain cells, is a "co-receptor" with the leptin receptor - meaning that both the leptin and LRP1 receptors need to work together to transmit leptin signals.
Leptin decides whether fat should be stored or used, resulting in lethargy or energy. When working properly, the hormone, which is made when body cells take in fat from food, travels to the brain to tamp down appetite...
While studying hormone receptors in laboratory mice, researchers at Mayo Clinic's campus in Florida and Washington University School of Medicine identified a new molecular player responsible for the regulation of appetite and metabolism.
The authors report that mice engineered not to express the lipoprotein receptor LRP1, in the brain's hypothalamus, began to eat uncontrollably, growing obese as well as lethargic. They found that LRP1, a major transporter of lipids and proteins into brain cells, is a "co-receptor" with the leptin receptor - meaning that both the leptin and LRP1 receptors need to work together to transmit leptin signals.
Leptin decides whether fat should be stored or used, resulting in lethargy or energy. When working properly, the hormone, which is made when body cells take in fat from food, travels to the brain to tamp down appetite...
Sunday, January 09, 2011
Thanks, Dad
Fathers, as well as mothers, can pass on a propensity to obesity if they themselves have been starved
THAT a gestating mother’s environment can have a permanent effect on the physiology of her offspring is well established. The children of Dutch women who were pregnant during the “Hunger Winter” of 1944, for example, suffer much higher rates of obesity, diabetes and cardiovascular disease than those born a year or two earlier. Similar observations in other famines, together with experiments on rodents, suggest this is an accidental consequence of an evolutionary adaptation to food scarcity. The offspring of starving mothers, anticipating hard times during their own future lives, adjust their metabolisms to hoard calories. If the hard times then go away, the result is a tendency to put on weight, with the unpleasant consequences that entails.
Part of this adaptation is a response by the embryo to the nutrition it receives through the placenta. In some cases, though, the unfertilised ovum itself is believed to be affected. Its DNA is reprogrammed, the theory goes, by a process called cytosine methylation. This switches genes on and off in a way that is maintained when DNA replicates during the process of cell division—and can thus be passed down the generations. It is, moreover, a process that could apply equally to the sperm of putative fathers who were starved around the time of mating.
There are hints that it does. In particular, a recent paper by Sheau-Fang Ng of the University of New South Wales showed that gene activity in the pancreases of mice sired by fat fathers is abnormal. That is significant because the pancreas makes insulin, which regulates blood sugar. Abnormal insulin levels cause diabetes...
THAT a gestating mother’s environment can have a permanent effect on the physiology of her offspring is well established. The children of Dutch women who were pregnant during the “Hunger Winter” of 1944, for example, suffer much higher rates of obesity, diabetes and cardiovascular disease than those born a year or two earlier. Similar observations in other famines, together with experiments on rodents, suggest this is an accidental consequence of an evolutionary adaptation to food scarcity. The offspring of starving mothers, anticipating hard times during their own future lives, adjust their metabolisms to hoard calories. If the hard times then go away, the result is a tendency to put on weight, with the unpleasant consequences that entails.
Part of this adaptation is a response by the embryo to the nutrition it receives through the placenta. In some cases, though, the unfertilised ovum itself is believed to be affected. Its DNA is reprogrammed, the theory goes, by a process called cytosine methylation. This switches genes on and off in a way that is maintained when DNA replicates during the process of cell division—and can thus be passed down the generations. It is, moreover, a process that could apply equally to the sperm of putative fathers who were starved around the time of mating.
There are hints that it does. In particular, a recent paper by Sheau-Fang Ng of the University of New South Wales showed that gene activity in the pancreases of mice sired by fat fathers is abnormal. That is significant because the pancreas makes insulin, which regulates blood sugar. Abnormal insulin levels cause diabetes...
Why are men getting so chubby?
British men are getting fatter than ever, faster than ever. Last week, Oxford University –scientists reported that the average man is more than a stone heavier — 17lb — than 20 years ago.
It would be easy to blame this dramatic increase on over-eating and lack of exercise, and leave it that. But the Oxford study showed that the explanation isn’t this simple.
Indeed, scientific research is revealing that a cocktail of unexpected factors is helping to drive the male obesity epidemic. These include genetics, pollution, stress, vanity, insomnia —and flabby friends.
A bigger Bond: Pierce Brosnan has piled on the pounds since playing the famous spy, right, in Die Another Day
There’s no doubt that British men are eating more. Over their 14-year study period, the Oxford researchers found that around 10.4lb of the extra weight men are carrying was due to extra calories.
But that did not explain the full 17?lb rise. And lack of exercise could only partly account for the difference, says the study leader, Dr Peter Scarborough.
By contrast, the extra 12lb the average woman gained over the same time is entirely explained by them eating more, according to the study, which was published in the British Journal of Nutrition.
This tallies with official statistics that show that nearly half of British men are overweight, compared with just a third of women, while a quarter of men are officially obese (compared with only 7 per cent in 1987).
The result is an epidemic of obesity-related diseases in men: cases of –diabetes have risen by almost a third since 2003, while in women they rose by less than a quarter. Overweight men also have much higher rates of cancer, stroke and heart disease.
More...
Confidence crisis: How the average overweight woman feels humiliated on a daily basis
How most size 12 women still believe they are too fat
Love yourself slim! Want to lose weight? The secret is to think you’re beautiful just the way you are right now
But if overeating and under-exercising are not solely to blame for men’s obesity and disease, what else might be making them fatter?
Research in this field is in its infancy compared with studies of women, but it indicates men have a unique –propensity to put on weight. In November, for example, U.S. –scientists reported they’d found a gene that causes weight gain in men, but not women.
The gene — Arrdc3 — is found in human fat and muscle, but seems to cause only men to become fat as they get older, says lead researcher Dr Parth Patwari of Brigham and Women’s Hospital in Massachusetts.
When he removed the gene from male mice, they no longer suffered from age-related weight gain; in fact, they showed a ‘striking –resistance’ to it. But when the gene was removed from female mice, it made no significant difference...
It would be easy to blame this dramatic increase on over-eating and lack of exercise, and leave it that. But the Oxford study showed that the explanation isn’t this simple.
Indeed, scientific research is revealing that a cocktail of unexpected factors is helping to drive the male obesity epidemic. These include genetics, pollution, stress, vanity, insomnia —and flabby friends.
A bigger Bond: Pierce Brosnan has piled on the pounds since playing the famous spy, right, in Die Another Day
There’s no doubt that British men are eating more. Over their 14-year study period, the Oxford researchers found that around 10.4lb of the extra weight men are carrying was due to extra calories.
But that did not explain the full 17?lb rise. And lack of exercise could only partly account for the difference, says the study leader, Dr Peter Scarborough.
By contrast, the extra 12lb the average woman gained over the same time is entirely explained by them eating more, according to the study, which was published in the British Journal of Nutrition.
This tallies with official statistics that show that nearly half of British men are overweight, compared with just a third of women, while a quarter of men are officially obese (compared with only 7 per cent in 1987).
The result is an epidemic of obesity-related diseases in men: cases of –diabetes have risen by almost a third since 2003, while in women they rose by less than a quarter. Overweight men also have much higher rates of cancer, stroke and heart disease.
More...
Confidence crisis: How the average overweight woman feels humiliated on a daily basis
How most size 12 women still believe they are too fat
Love yourself slim! Want to lose weight? The secret is to think you’re beautiful just the way you are right now
But if overeating and under-exercising are not solely to blame for men’s obesity and disease, what else might be making them fatter?
Research in this field is in its infancy compared with studies of women, but it indicates men have a unique –propensity to put on weight. In November, for example, U.S. –scientists reported they’d found a gene that causes weight gain in men, but not women.
The gene — Arrdc3 — is found in human fat and muscle, but seems to cause only men to become fat as they get older, says lead researcher Dr Parth Patwari of Brigham and Women’s Hospital in Massachusetts.
When he removed the gene from male mice, they no longer suffered from age-related weight gain; in fact, they showed a ‘striking –resistance’ to it. But when the gene was removed from female mice, it made no significant difference...
How the brain's use of fatty acids is linked to obesity
Researchers have established a link between how lipid sensing and metabolism in the brain relate to the regulation of energy balance and body weight.
Hong Wang of University of Colorado created mice with a deficiency of lipoprotein lipase (LPL) in neurons, and observed that the mouse models ate less and they became sedentary.
"This work may have important impact in understanding the causes of obesity and providing new treatments for this epidemic of our time," said Robert H. Eckel.
These mice became obese on a standard chow diet between three and six months. The research also looked at which areas of the brain have the greatest impact on regulating body weight...
Hong Wang of University of Colorado created mice with a deficiency of lipoprotein lipase (LPL) in neurons, and observed that the mouse models ate less and they became sedentary.
"This work may have important impact in understanding the causes of obesity and providing new treatments for this epidemic of our time," said Robert H. Eckel.
These mice became obese on a standard chow diet between three and six months. The research also looked at which areas of the brain have the greatest impact on regulating body weight...
Tree Bark Drug To Fight Obesity
A new drug which contains an element found in the bark of trees may be able to provide new treatments for obesity as well as a number of other major illnesses. The compound, Betulin, which is found in abundance in the bark of birch trees, is able to target genes that produce fats in the blood stream.
In trials it has helped to prevent obesity induced by dietary factors as well as reducing the risk of both diabetes and heart disease. Mice that were fed an atypical high-fat diet when then treated with betulin. The compound caused the mice led to increase the rate at which they burned calories...
In trials it has helped to prevent obesity induced by dietary factors as well as reducing the risk of both diabetes and heart disease. Mice that were fed an atypical high-fat diet when then treated with betulin. The compound caused the mice led to increase the rate at which they burned calories...
Sunday, January 02, 2011
Have heart disease? Perhaps dad's diet is to blame
For the past few years, a slew of studies have focused attention on the role that a pregnant woman's diet has on the future health of her offspring. I previously warned women off doughnuts and Big Macs in this article citing research showing that pregnant women who dined on junk food could increase their baby's chances of developing diabetes and heart disease later in life.
That's because certain environmental factors -- like how much weight a woman gains when she's pregnant, what she eats and what chemicals she's exposed to -- actually affect how her baby's genes are programmed in the womb.
Well, now it's time for dads to share some of the blame for faulty programming that wires kids for obesity and a host of other health ills. A study published last week in the journal Cell suggests that what a father eats before his offspring are created can have some influence on fetal programming for disease risk.
At least father mice, since that's what the researchers studied...
That's because certain environmental factors -- like how much weight a woman gains when she's pregnant, what she eats and what chemicals she's exposed to -- actually affect how her baby's genes are programmed in the womb.
Well, now it's time for dads to share some of the blame for faulty programming that wires kids for obesity and a host of other health ills. A study published last week in the journal Cell suggests that what a father eats before his offspring are created can have some influence on fetal programming for disease risk.
At least father mice, since that's what the researchers studied...
Japanese firm partners with local researchers to fight obesity
"In labs, we've cured obesity and diabetes in mice hundreds of times," Smith said. "But not all the things that work in mice work in people."...
Officials at Orlando's Sanford-Burnham Research Institute and Florida Hospital on Monday announced a major partnership with Asia's largest pharmaceutical company — an alliance that will explore new ways to treat obesity.
Takeda Pharmaceuticals, a Japanese firm that has made major investments in diabetes and obesity research, inked a two-year deal with the nonprofit biomedical research facility at Lake Nona and its joint venture with Florida Hospital, the Translational Research Institute for Metabolism and Diabetes.
The two-year collaboration includes research funding from Takeda, but officials involved in the agreement would not disclose the terms of the deal. However, Sanford-Burnham officials said the new alliance is one of the largest and most ambitious research partnerships that Takeda has conducted with the not-for-profit sector.
"In terms of their discovery types of partnerships, this is one of the most significant that they have ever established outside of Japan," said Dr. Daniel Kelly, scientific director of Sanford-Burnham's Lake Nona campus.
"We view this collaboration as an opportunity to further Takeda's goal of identifying targets for new therapeutics to treat obesity and its negative health consequences, including metabolic syndrome, diabetes and heart disease," said Dr. Paul Chapman, head of Takeda's pharmaceutical research division.
The partnership is a significant step for Sanford-Burnham's Lake Nona campus, said Russell Allen, president of BioFlorida, the state's biomedical industry association.
"Takeda is a large, well-known company," he said. "It does help validate that Sanford-Burnham in Orlando is conducting strong science because Takeda is not going to partner with just anyone."
Although most obesity drugs on the market today target the brain — in hopes of controlling a person's appetite — those types of drugs often have serious side effects, including depression. Researchers at Sanford Burnham and the Translational Research Institute are taking another approach: Trying to make a person's muscles burn more fat.
"We're looking at ways to turn on fat-burning," said Dr. Steven Smith, scientific director at the Translational Research Institute. "The idea is that we can help people lose weight by turning on the fat-burning and fat-oxidation mechanisms."
The earliest stages of the research will include studying the muscles of those who are obese and learning what makes their muscles different from everyone else's. That information will be used by scientists at Sanford-Burnham and Takeda to do lab research.
Officials at the three organizations began discussing a potential partnership in early 2010. Being able to test ideas on people — instead of lab mice — made the collaboration attractive to the scientists involved.
"In labs, we've cured obesity and diabetes in mice hundreds of times," Smith said....
Officials at Orlando's Sanford-Burnham Research Institute and Florida Hospital on Monday announced a major partnership with Asia's largest pharmaceutical company — an alliance that will explore new ways to treat obesity.
Takeda Pharmaceuticals, a Japanese firm that has made major investments in diabetes and obesity research, inked a two-year deal with the nonprofit biomedical research facility at Lake Nona and its joint venture with Florida Hospital, the Translational Research Institute for Metabolism and Diabetes.
The two-year collaboration includes research funding from Takeda, but officials involved in the agreement would not disclose the terms of the deal. However, Sanford-Burnham officials said the new alliance is one of the largest and most ambitious research partnerships that Takeda has conducted with the not-for-profit sector.
"In terms of their discovery types of partnerships, this is one of the most significant that they have ever established outside of Japan," said Dr. Daniel Kelly, scientific director of Sanford-Burnham's Lake Nona campus.
"We view this collaboration as an opportunity to further Takeda's goal of identifying targets for new therapeutics to treat obesity and its negative health consequences, including metabolic syndrome, diabetes and heart disease," said Dr. Paul Chapman, head of Takeda's pharmaceutical research division.
The partnership is a significant step for Sanford-Burnham's Lake Nona campus, said Russell Allen, president of BioFlorida, the state's biomedical industry association.
"Takeda is a large, well-known company," he said. "It does help validate that Sanford-Burnham in Orlando is conducting strong science because Takeda is not going to partner with just anyone."
Although most obesity drugs on the market today target the brain — in hopes of controlling a person's appetite — those types of drugs often have serious side effects, including depression. Researchers at Sanford Burnham and the Translational Research Institute are taking another approach: Trying to make a person's muscles burn more fat.
"We're looking at ways to turn on fat-burning," said Dr. Steven Smith, scientific director at the Translational Research Institute. "The idea is that we can help people lose weight by turning on the fat-burning and fat-oxidation mechanisms."
The earliest stages of the research will include studying the muscles of those who are obese and learning what makes their muscles different from everyone else's. That information will be used by scientists at Sanford-Burnham and Takeda to do lab research.
Officials at the three organizations began discussing a potential partnership in early 2010. Being able to test ideas on people — instead of lab mice — made the collaboration attractive to the scientists involved.
"In labs, we've cured obesity and diabetes in mice hundreds of times," Smith said....
Obesity caused by what you breathe?
Diabetes. Asthma. Obesity. All are on the rise. What if they're all caused by the same thing?
At least one study found that air pollution — known to contribute to asthma — also spurs both obesity and diabetes in young mice, suggesting that it may also contribute to the ubiquitous problems in humans.
Ohio State researchers found that young mice exposed to air pollution had larger and more fat cells in their abdominal area and higher blood sugar levels than mice eating the same diet but breathing clean air...
At least one study found that air pollution — known to contribute to asthma — also spurs both obesity and diabetes in young mice, suggesting that it may also contribute to the ubiquitous problems in humans.
Ohio State researchers found that young mice exposed to air pollution had larger and more fat cells in their abdominal area and higher blood sugar levels than mice eating the same diet but breathing clean air...
Sunday, December 26, 2010
VITAMIN D REDUCES OBESITY-INDUCED UTERINE CANCER
FINDINGS FROM AN ANIMAL study by Georgetown researchers suggest obese women can reduce their risk of endometrial cancer by taking vitamin D supplements.
Scientists from Georgetown’s Lombardi Comprehensive Cancer Center recently showed that 67 percent of obese mice fed a regular diet developed this cancer, versus only 25 percent of obese mice fed a vitamin D-supplemented diet...
Scientists from Georgetown’s Lombardi Comprehensive Cancer Center recently showed that 67 percent of obese mice fed a regular diet developed this cancer, versus only 25 percent of obese mice fed a vitamin D-supplemented diet...
Could tea help with obesity treatment?
People undergoing obesity treatment could benefit from drinking tea.
A recent research project has revealed that tea can help to restrict weight gain and limit the negative health impact of fatty foods.
Conducted at Kobe University in Japan, the study looked at a group of mice fed either a normal diet or a high-fat diet.
The mice were also given water, black tea or green tea over a 14-week period.
Results showed that the mice that were drinking tea had suppressed body weight gain in comparison to the group on water.
In addition, black tea was found to counteract the harmful effects of the fat on the blood.
Dr Carrie Ruxton from the industry-backed Tea Advisory Panel explained: "This study is good news for tea drinkers, particularly those who drink black tea.
"Though the findings need to be confirmed in human studies...
A recent research project has revealed that tea can help to restrict weight gain and limit the negative health impact of fatty foods.
Conducted at Kobe University in Japan, the study looked at a group of mice fed either a normal diet or a high-fat diet.
The mice were also given water, black tea or green tea over a 14-week period.
Results showed that the mice that were drinking tea had suppressed body weight gain in comparison to the group on water.
In addition, black tea was found to counteract the harmful effects of the fat on the blood.
Dr Carrie Ruxton from the industry-backed Tea Advisory Panel explained: "This study is good news for tea drinkers, particularly those who drink black tea.
"Though the findings need to be confirmed in human studies...
Researchers Turn White Fat to Energy-Burning Brown Fat in Mice
Certain cells in white fat can be changed into energy-burning brown fat, according to an animal study that might one day lead to new treatments for obesity, researchers report.
In tests on mice, a team at the Joslin Diabetes Center in Boston found that exposure to a protein called BMP-7 caused progenitor cells in subcutaneous (just beneath the skin) white fat tissue and skeletal muscle to turn into brown fat cells...
In tests on mice, a team at the Joslin Diabetes Center in Boston found that exposure to a protein called BMP-7 caused progenitor cells in subcutaneous (just beneath the skin) white fat tissue and skeletal muscle to turn into brown fat cells...
Tuesday, December 21, 2010
Novel Weight-Loss Therapies? Scientists Identify Cells in Mice That Can Transform Into Energy-Burning Brown Fat
In some adults, the white fat cells that we all stockpile so readily are supplemented by a very different form of fat -- brown fat cells, which can offer the neat trick of burning energy rather than storing it. Researchers at Joslin Diabetes Center, which last year led the way in demonstrating an active role for brown fat in adults, now have identified progenitor cells in mouse white fat tissue and skeletal muscle that can be transformed into brown fat cells...
Monday, December 20, 2010
Top 100 Stories of 2010 #8: Obesity Reaches Epidemic Proportions
On the research front, meanwhile, investigators are making some progress in grasping obesity’s causes. A provocative study published in Science in April 2010 suggests that a change in the bacterial population of the gut contributes to the risk of metabolic syndrome, which is characterized by elevated weight, blood pressure, blood sugar, and blood fat. Researchers led by Emory University pathologist Andrew Gewirtz found that mice genetically deficient in an immune system receptor have altered gut bacteria, eat more than normal mice do, and develop features of metabolic syndrome. However, Gewirtz says it is “unlikely that there will be a single causative bacterium for obesity as there
is for ulcers.”
New research suggests viruses could be the cause of the obesity epidemic
THE obesity epidemic seen in humans and their pets may be caused by more than rubbish diets and lack of exercise.
Some scientists think it may be due to a combination of issues, including viruses or something else that affects cells or organs.
This is opposed to the commonly held belief based on poor Western lifestyles that feature over-eating, little exercise and fatty foods.
Scientists' curiosity was triggered when they noticed laboratory rats and mice on strict diets had put on weight just as domestic pets and feral animals living around humans had...
Some scientists think it may be due to a combination of issues, including viruses or something else that affects cells or organs.
This is opposed to the commonly held belief based on poor Western lifestyles that feature over-eating, little exercise and fatty foods.
Scientists' curiosity was triggered when they noticed laboratory rats and mice on strict diets had put on weight just as domestic pets and feral animals living around humans had...
Too fat? Study fingers one "thrifty gene" suspect
Looking beyond obvious causes of obesity like overeating, scientists said on Wednesday they may have found a gene that also plays a role, one that helped our ancestors survive famines.
Targeting this thrifty gene and others with diagnostic tests and drugs offers another way to fight the global epidemic of obesity, the researchers said.
Mice bred to lack this gene, known as CRTC3, can eat a high-fat diet without gaining weight, while normal mice on the same diet grow plump, the researchers found...
Targeting this thrifty gene and others with diagnostic tests and drugs offers another way to fight the global epidemic of obesity, the researchers said.
Mice bred to lack this gene, known as CRTC3, can eat a high-fat diet without gaining weight, while normal mice on the same diet grow plump, the researchers found...
Scientists Raise Fat-Burning Levels in Mice
Deleting the receptor of a protein known to promote obesity allowed mice to burn more fat, researchers report.
The role of the ghrelin protein in appetite and energy balance was discovered in 1999. This new finding suggests that ghrelin may not be as critical to energy expenditure as its cellular receptor, called growth hormone secretagogue receptor (GHS-R), explained Dr. Yuxiang Sun, of the Baylor College of Medicine in Houston.
That means that GHS-R might make a better target for treating obesity in humans.
In this study, Sun and colleagues found that deleting GHS-R from the body cells of mice prevented obesity by diminishing so-called "white fat" tissue and activating "brown fat" tissue, thereby increasing the production of fat-burning body heat...
The role of the ghrelin protein in appetite and energy balance was discovered in 1999. This new finding suggests that ghrelin may not be as critical to energy expenditure as its cellular receptor, called growth hormone secretagogue receptor (GHS-R), explained Dr. Yuxiang Sun, of the Baylor College of Medicine in Houston.
That means that GHS-R might make a better target for treating obesity in humans.
In this study, Sun and colleagues found that deleting GHS-R from the body cells of mice prevented obesity by diminishing so-called "white fat" tissue and activating "brown fat" tissue, thereby increasing the production of fat-burning body heat...
Tuesday, December 14, 2010
Deleting Ghrelin Receptor, but Not Ghrelin, Turns Up Fat-Burning Thermostat
Deleting the receptor, not the protein ghrelin itself, turns up the body's fat-burning thermostat, giving aging mice an exothermic boost toward a svelte physique, researchers reported at the American Society of Cell Biology's 50th Annual Meeting in Philadelphia.
The protein's receptor, growth hormone secretagogue receptor (GHS-R), might make a better target than ghrelin for treating obesity, according to Yuxiang Sun, M.D., Ph.D., of the Baylor College of Medicine in Houston, TX.
Sun said that experimentally deleting the receptor from the body cells of laboratory mice prevented obesity by diminishing white adipose tissues and activating brown adipose tissue, thereby increasing heat production.
The new finding that ghrelin may not be as critical to energy expenditure as its receptor, GHS-R, came from research on body temperature regulation at Baylor, Sun explained. GHS-R acts as the "lock" for the "key-like" ligand ghrelin to dock; GHS-R subsequently activates down-stream metabolic signal pathways...
The protein's receptor, growth hormone secretagogue receptor (GHS-R), might make a better target than ghrelin for treating obesity, according to Yuxiang Sun, M.D., Ph.D., of the Baylor College of Medicine in Houston, TX.
Sun said that experimentally deleting the receptor from the body cells of laboratory mice prevented obesity by diminishing white adipose tissues and activating brown adipose tissue, thereby increasing heat production.
The new finding that ghrelin may not be as critical to energy expenditure as its receptor, GHS-R, came from research on body temperature regulation at Baylor, Sun explained. GHS-R acts as the "lock" for the "key-like" ligand ghrelin to dock; GHS-R subsequently activates down-stream metabolic signal pathways...
Monday, December 13, 2010
Air pollution may increase risk of type 2 diabetes
Exposure to air pollution may increase the risk of developing obesity-related insulin resistance, which often progresses into type 2 diabetes, according to new research from Ohio State University.
Air pollution has been connected to a broad range of health problems, including cardiovascular dysfunction and certain types of cancer. However, the findings of the new research, which were published in the journal Arteriosclerosis, Thrombosis, and Vascular Biology are the first to indicate a potential link to diabetes.
For the study, researchers exposed adolescent mice to the sort of fine particulate air pollution that is commonly associated with automobile exhaust. When these animals reached adulthood, researchers found that they had higher levels of abdominal fat than normal mice.
"This is one of the first, if not the first, study to show that these fine particulates directly cause inflammation and changes in fat cells, both of which increase the risk for Type 2 diabetes," said Qinghua Sun, who led the investigation...
Air pollution has been connected to a broad range of health problems, including cardiovascular dysfunction and certain types of cancer. However, the findings of the new research, which were published in the journal Arteriosclerosis, Thrombosis, and Vascular Biology are the first to indicate a potential link to diabetes.
For the study, researchers exposed adolescent mice to the sort of fine particulate air pollution that is commonly associated with automobile exhaust. When these animals reached adulthood, researchers found that they had higher levels of abdominal fat than normal mice.
"This is one of the first, if not the first, study to show that these fine particulates directly cause inflammation and changes in fat cells, both of which increase the risk for Type 2 diabetes," said Qinghua Sun, who led the investigation...
Monday, December 06, 2010
Artificial light at night may cause obesity
...The present study compares three groups of lab mice. One was exposed to a "regular day" of 16 light hours and eight hours of dark. A second group was in continuous light for 24 hours and the third group was given regular light for 16 hours followed by eight hours of dimmed light. The three groups were placed in these conditions over the course of eight weeks and were given equal quantities of food.
The results show that the mice experiencing dimmed light and those exposed to 24 hours of light gained about 12 grams of body mass, while the mice exposed to the "regular day" only put on about eight grams of extra body mass - close to 50 percent less than the others.
The researchers observed that there was no difference in the amounts of food that all the mice ate, or in the extent of physical activity (monitored as locomotor activity). The lab tests also showed drastically reduced glucose tolerance in those mice exposed to LAN.
Another finding, which led to the second stage of the study, showed a significant difference between the groups in their timing of eating: The mice exposed to dimmed light ate 55% of their food during the "night" hours while those experiencing "regular days" ate only 36.5% of their food at night. This prompted the researchers to see whether this was the cause of the marked differences in body mass gain.
To do so, they gave the group of mice enjoying "regular days" and those exposed to dimmed light hours, three different options: Unlimited eating times; food only during the light hours; and food only during the "night" hours. There was no need to include the third group in this step of the research, as they did not have any "night" hours.
Nighttime TV can cause obesity
Once eating was limited to daytime only (which is when mice normally eat their food) or nighttime only (when they do not normally eat), there was no difference in body mass weight gain between the groups.
Haim explains that the study strengthens earlier findings by other researchers showing that exposure to LAN interferes with the production of melatonin - a hormone produced in the pineal gland in the brain under dark conditions at night. This interference causes changes in the body's cyclical functions and is what caused the mice to eat at abnormal hours...
The results show that the mice experiencing dimmed light and those exposed to 24 hours of light gained about 12 grams of body mass, while the mice exposed to the "regular day" only put on about eight grams of extra body mass - close to 50 percent less than the others.
The researchers observed that there was no difference in the amounts of food that all the mice ate, or in the extent of physical activity (monitored as locomotor activity). The lab tests also showed drastically reduced glucose tolerance in those mice exposed to LAN.
Another finding, which led to the second stage of the study, showed a significant difference between the groups in their timing of eating: The mice exposed to dimmed light ate 55% of their food during the "night" hours while those experiencing "regular days" ate only 36.5% of their food at night. This prompted the researchers to see whether this was the cause of the marked differences in body mass gain.
To do so, they gave the group of mice enjoying "regular days" and those exposed to dimmed light hours, three different options: Unlimited eating times; food only during the light hours; and food only during the "night" hours. There was no need to include the third group in this step of the research, as they did not have any "night" hours.
Nighttime TV can cause obesity
Once eating was limited to daytime only (which is when mice normally eat their food) or nighttime only (when they do not normally eat), there was no difference in body mass weight gain between the groups.
Haim explains that the study strengthens earlier findings by other researchers showing that exposure to LAN interferes with the production of melatonin - a hormone produced in the pineal gland in the brain under dark conditions at night. This interference causes changes in the body's cyclical functions and is what caused the mice to eat at abnormal hours...
Study Finds Possible Link To Obesity
...Childs' discovery has to do with leptin, a hormone that's known to control appetite by acting on specific neurons in the brain. Past studies of leptin have focused on leptin's function within the brain. Childs' study focused on leptin receptors that are on growth hormone cells in the pituitary, which, in addition to stimulating growth of bones and muscle, play a key role in breaking down fat.
In Childs' study, the leptin receptor gene in growth hormone cells was removed in mice. The original purpose was to observe the effects on reproduction, because both leptin and growth hormone are known to be involved in the timing of puberty. However, Childs noticed that whereas puberty was normal, the male mice were becoming overweight as they reached adulthood and the female mice became overweight several months later.
"Tests of serum leptin and leptin receptor levels in the brain suggested that normal leptin is available to effectively control their appetite, and yet they still are gaining weight," Childs said of the genetically altered mice.
She concluded that the obesity was caused by removing the leptin receptor on the mice's growth hormone cells (pituitary somatotropes).
"This is very new; everyone had thought that leptin's most important functions were in the brain to control appetite," she said.
The overweight mice had 60 percent fewer growth hormone cells than the control mice, which means they did not produce enough growth hormone to break down fat as effectively as the control mice. This shows how important leptin is to the maintenance of a normal population of growth hormone cells. It also shows how important growth hormone is to the optimization of body composition including fat...
In Childs' study, the leptin receptor gene in growth hormone cells was removed in mice. The original purpose was to observe the effects on reproduction, because both leptin and growth hormone are known to be involved in the timing of puberty. However, Childs noticed that whereas puberty was normal, the male mice were becoming overweight as they reached adulthood and the female mice became overweight several months later.
"Tests of serum leptin and leptin receptor levels in the brain suggested that normal leptin is available to effectively control their appetite, and yet they still are gaining weight," Childs said of the genetically altered mice.
She concluded that the obesity was caused by removing the leptin receptor on the mice's growth hormone cells (pituitary somatotropes).
"This is very new; everyone had thought that leptin's most important functions were in the brain to control appetite," she said.
The overweight mice had 60 percent fewer growth hormone cells than the control mice, which means they did not produce enough growth hormone to break down fat as effectively as the control mice. This shows how important leptin is to the maintenance of a normal population of growth hormone cells. It also shows how important growth hormone is to the optimization of body composition including fat...
Polluted air 'ups obesity risk in young animals'
A new research showed that exposure to polluted air early in life led to an accumulation of abdominal fat and insulin resistance in mice even if they ate a normal diet.
Animals exposed to the fine-particulate air pollution had larger and more fat cells in their abdominal area and higher blood sugar levels than did animals eating the same diet but breathing clean air.
Researchers exposed the mice to the polluted air for six hours a day, five days a week for 10 weeks beginning when the animals were 3 weeks old. This time frame roughly matches the toddler years to late adolescence in humans...
Animals exposed to the fine-particulate air pollution had larger and more fat cells in their abdominal area and higher blood sugar levels than did animals eating the same diet but breathing clean air.
Researchers exposed the mice to the polluted air for six hours a day, five days a week for 10 weeks beginning when the animals were 3 weeks old. This time frame roughly matches the toddler years to late adolescence in humans...
A couch-potato mouse? Sanford-Burnham researchers say it holds key to obesity
Scientists at Orlando's Sanford-Burnham Medical Research Institute have come up with an unusual new model for studying the way muscles work and how that relates to obesity: a couch-potato mouse.
In a new study being released today in the journal Cell Metabolism, Dr. Daniel Kelly and a team of colleagues at Sanford-Burnham's Lake Nona campus created laboratory mice with very low levels of a protein called PGC-1 in their muscles.
Kelly and his team were surprised to find that the mice they engineered with the low protein levels were not obese or overweight. Instead, they looked normal and walked around without problems.
But put them on a treadmill and they could only run short distances. While the average mouse could last 170 minutes on a treadmill, the couch-potato mouse ran only 6.6 minutes...
In a new study being released today in the journal Cell Metabolism, Dr. Daniel Kelly and a team of colleagues at Sanford-Burnham's Lake Nona campus created laboratory mice with very low levels of a protein called PGC-1 in their muscles.
Kelly and his team were surprised to find that the mice they engineered with the low protein levels were not obese or overweight. Instead, they looked normal and walked around without problems.
But put them on a treadmill and they could only run short distances. While the average mouse could last 170 minutes on a treadmill, the couch-potato mouse ran only 6.6 minutes...
Sunday, November 28, 2010
Fat Yet Muscular Mouse Provides Clues To Improving Cardiovascular Health
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...
"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...
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...
Virus 'link' to childhood obesity
A virus which causes respiratory infections has been linked to childhood obesity, in a study that is likely to reignite a controversial debate.
Previous animal research has implicated common viruses in weight gain, but the evidence has been disputed.
The latest study, in Pediatrics, found that obese children with antibodies specific to a certain virus weighed 35lbs (15.8kg) more than those without.
Nothing has yet been proven on this theory, say UK experts.
Previous research has shown that chicken or mice injected with similar types of viruses showed a statistically significant weight gain...
Previous animal research has implicated common viruses in weight gain, but the evidence has been disputed.
The latest study, in Pediatrics, found that obese children with antibodies specific to a certain virus weighed 35lbs (15.8kg) more than those without.
Nothing has yet been proven on this theory, say UK experts.
Previous research has shown that chicken or mice injected with similar types of viruses showed a statistically significant weight gain...
Study Clarifies Obesity-Infertility Link
Being obese has long been linked to infertility in females, but researchers may have been wrong about how the link was forged, a new study suggests.
Doctors and scientists have thought that the fertility problems were caused by resistance to the hormone insulin. Chronically high levels of insulin often accompany obesity, eventually making muscles and other tissues impervious to the hormone’s signals.
A new study in mice shows that the pituitary gland, which helps regulate the release of fertility-associated hormones, remains sensitive to insulin. But in obese mice, insulin’s constant signaling to release the fertility hormones leads to an overabundance of those hormones, and consequently infertility, researchers report in the Sept. 8 Cell Metabolism.
The discovery firmly ties metabolism to fertility in an unexpected way and may have implications for treating women with a condition known as polycystic ovary syndrome, which is characterized by abnormal menstrual cycles and is often associated with obesity and type 2 diabetes...
Doctors and scientists have thought that the fertility problems were caused by resistance to the hormone insulin. Chronically high levels of insulin often accompany obesity, eventually making muscles and other tissues impervious to the hormone’s signals.
A new study in mice shows that the pituitary gland, which helps regulate the release of fertility-associated hormones, remains sensitive to insulin. But in obese mice, insulin’s constant signaling to release the fertility hormones leads to an overabundance of those hormones, and consequently infertility, researchers report in the Sept. 8 Cell Metabolism.
The discovery firmly ties metabolism to fertility in an unexpected way and may have implications for treating women with a condition known as polycystic ovary syndrome, which is characterized by abnormal menstrual cycles and is often associated with obesity and type 2 diabetes...
Poor biological clock leads to obesity
UC San Diego biologists have discovered biological clocks of mammals are related to development of obesity and diabetes.
It also raises the possibility that some of the rise in diabetes could be a consequence of disturbances in sleep-wake cycles from our increasingly around-the-clock lifestyles.
"We know that mice that don't have good biological clocks tend to develop diabetes and obesity. And we know that mice that have developed diabetes and obesity tend not to have very good biological clocks," Nature quoted Steve Kay at UC San Diego, as saying.
"But what we found that's so significant is that a particular biological clock protein, cryptochrome, is actually regulating how the hormone that regulates glucose production in the liver works in a very specific way," he added.
The study also indicates why shift workers, whose biological clocks are often out of step, also have a greater risk of developing obesity and insulin resistance...
It also raises the possibility that some of the rise in diabetes could be a consequence of disturbances in sleep-wake cycles from our increasingly around-the-clock lifestyles.
"We know that mice that don't have good biological clocks tend to develop diabetes and obesity. And we know that mice that have developed diabetes and obesity tend not to have very good biological clocks," Nature quoted Steve Kay at UC San Diego, as saying.
"But what we found that's so significant is that a particular biological clock protein, cryptochrome, is actually regulating how the hormone that regulates glucose production in the liver works in a very specific way," he added.
The study also indicates why shift workers, whose biological clocks are often out of step, also have a greater risk of developing obesity and insulin resistance...
U.S. animal study shows vitamin D protects against obesity-induced endometrial cancer
Findings from an animal study suggest that obese women can reduce their increased risk of endometrial disease if they take vitamin D supplements, say researchers at the Georgetown University Lombardi Comprehensive Cancer Center.
The scientists report in Cancer Prevention Research published online Tuesday that 25 percent of obese mice fed a vitamin D supplemented diet developed endometrial cancer, while 67 percent of obese mice not treated with the vitamin developed cancer. They also report that vitamin D offered no protective effects for normal weight mice; whether or not they used the vitamin, about 60 percent of these mice developed cancer.
All of the mice were genetically predisposed to develop endometrial cancer, because they were missing one of their two PTEN tumor suppressor genes, loss of which is strongly linked to development of human endometrial cancer. Obesity is also a strong known risk factor, researchers say.
"Vitamin D has been shown to be helpful in a number of cancers, but for endometrial cancer, our study suggests it protects only against cancer that develops due to obesity," says the study's lead investigator, Leena Hilakivi-Clarke, a professor of Oncology. "Still, if these results are confirmed in women, use of vitamin D may be a wonderfully simple way to reduce endometrial cancer risk...
The scientists report in Cancer Prevention Research published online Tuesday that 25 percent of obese mice fed a vitamin D supplemented diet developed endometrial cancer, while 67 percent of obese mice not treated with the vitamin developed cancer. They also report that vitamin D offered no protective effects for normal weight mice; whether or not they used the vitamin, about 60 percent of these mice developed cancer.
All of the mice were genetically predisposed to develop endometrial cancer, because they were missing one of their two PTEN tumor suppressor genes, loss of which is strongly linked to development of human endometrial cancer. Obesity is also a strong known risk factor, researchers say.
"Vitamin D has been shown to be helpful in a number of cancers, but for endometrial cancer, our study suggests it protects only against cancer that develops due to obesity," says the study's lead investigator, Leena Hilakivi-Clarke, a professor of Oncology. "Still, if these results are confirmed in women, use of vitamin D may be a wonderfully simple way to reduce endometrial cancer risk...
Sunday, September 05, 2010
Reset your body clock? Maybe, new study suggests
Scientists have used experimental drugs being developed by Pfizer to reset and restart the body clock of mice in a lab and say their work may offer clues on a range of human disorders, from jetlag to bipolar disorder.
The drugs, which are not yet available in a form suitable for humans and could take many years to develop into human medicines, work by altering the activity of an enzyme which helps set the speed of the body clock.
Researchers say they could potentially restore rhythms in people whose body clocks are messed up by shift work, or in psychiatric disorders like depression, and may even have implications for metabolic problems such as obesity...
The drugs, which are not yet available in a form suitable for humans and could take many years to develop into human medicines, work by altering the activity of an enzyme which helps set the speed of the body clock.
Researchers say they could potentially restore rhythms in people whose body clocks are messed up by shift work, or in psychiatric disorders like depression, and may even have implications for metabolic problems such as obesity...
'Sprouty' protein could be a therapeutic target for obesity, osteoporosis
A newly discovered protein termed as 'sprouty' protein could be the answer to obesity and/or osteoporosis, as well as diabetes, osteoarthritis and heart disease.
Scientists from Maine report findings on the protein that could regulate body fat and bone mass.
They found that the more of this protein that the transgenic mice expressed, the leaner and stronger they became, and when mice with low levels of the Sprouty protein were made to express more of it, they lost weight and increased bone density.
Results showed that the mice with the deleted Sprouty gene had increased body fat and loss of bone mass similar to osteoporosis as compared to normal mice. Adding more Sprouty protein then reversed bone loss. The group with excess Sprouty expression produced lean mice with increased bone mass...
Scientists from Maine report findings on the protein that could regulate body fat and bone mass.
They found that the more of this protein that the transgenic mice expressed, the leaner and stronger they became, and when mice with low levels of the Sprouty protein were made to express more of it, they lost weight and increased bone density.
Results showed that the mice with the deleted Sprouty gene had increased body fat and loss of bone mass similar to osteoporosis as compared to normal mice. Adding more Sprouty protein then reversed bone loss. The group with excess Sprouty expression produced lean mice with increased bone mass...
Eating at right time a must to keep obesity at bay
Eating less and exercising more to keep obesity at bay might not be enough. Now there is new evidence to show that eating at the right time is also a must for weight loss.
A Northwestern University study has found that eating at irregular times, especially when the body wants to sleep, influences weight gain.
"How or why a person gains weight is very complicated, but it clearly is not just calories in and calories out," said Fred Turek, neurobiology and physiology professor at the Weinberg College of Arts and Sciences and director of the Centre for Sleep and Circadian Biology.
The findings could have implications for developing strategies to combat obesity in humans, as the US and the world battle what has been called an "obesity epidemic". More than 300 million adults worldwide are obese, including more than a third of American adults.
"Their schedules force them to eat at times that conflict with their natural body rhythms. This was one piece of evidence that got us thinking -- eating at the wrong time might be contributing to weight gain," says Arble.
Simply modifying the time of feeding alone can greatly affect body weight, the researchers found, says a university statement.
Mice that were fed a high-fat diet during normal sleeping hours gained significantly more weight (a 48 percent increase) than mice eating the same type and amount of food during naturally wakeful hours (a 20 percent increase).
A Northwestern University study has found that eating at irregular times, especially when the body wants to sleep, influences weight gain.
"How or why a person gains weight is very complicated, but it clearly is not just calories in and calories out," said Fred Turek, neurobiology and physiology professor at the Weinberg College of Arts and Sciences and director of the Centre for Sleep and Circadian Biology.
The findings could have implications for developing strategies to combat obesity in humans, as the US and the world battle what has been called an "obesity epidemic". More than 300 million adults worldwide are obese, including more than a third of American adults.
"Their schedules force them to eat at times that conflict with their natural body rhythms. This was one piece of evidence that got us thinking -- eating at the wrong time might be contributing to weight gain," says Arble.
Simply modifying the time of feeding alone can greatly affect body weight, the researchers found, says a university statement.
Mice that were fed a high-fat diet during normal sleeping hours gained significantly more weight (a 48 percent increase) than mice eating the same type and amount of food during naturally wakeful hours (a 20 percent increase).
Mouse Study May Help Explain Fish Oil's Benefits
Feeding obese mice omega-3 fatty acids reduced inflammation that can lead to diabetes, a new study finds.
Fish oil supplements that contain high levels of omega-3 fatty acids are one of the most popular dietary supplements in the United States. While omega-3 fatty acids are widely believed to be beneficial, exactly how they work hasn't been well understood, said study co-author Saswata Talukdar, a post-doctoral fellow at University of California, San Diego.
By studying fat tissue in the mice consuming fish oil, researchers found omega-3 fatty acids seem to act on a particular receptor on cells, GPR120, which, when activated, blocks inflammatory processes.
Chronic inflammation can lead to insulin resistance, a precursor to diabetes.
Therefore, "if we can fix the inflammation part, it's possible that we could prevent insulin resistance or even ameliorate diabetes," Talukdar explained.
The study was published in the Sept. 3 issue of the journal Cell...
Fish oil supplements that contain high levels of omega-3 fatty acids are one of the most popular dietary supplements in the United States. While omega-3 fatty acids are widely believed to be beneficial, exactly how they work hasn't been well understood, said study co-author Saswata Talukdar, a post-doctoral fellow at University of California, San Diego.
By studying fat tissue in the mice consuming fish oil, researchers found omega-3 fatty acids seem to act on a particular receptor on cells, GPR120, which, when activated, blocks inflammatory processes.
Chronic inflammation can lead to insulin resistance, a precursor to diabetes.
Therefore, "if we can fix the inflammation part, it's possible that we could prevent insulin resistance or even ameliorate diabetes," Talukdar explained.
The study was published in the Sept. 3 issue of the journal Cell...
Born lazy: how genes dictate our love of exercise
Researchers discovered that the love of wanting to keep fit is in your genes and can be passed on from generation to generation.
Conversely, the same is true about being a couch potato.
In the future, people who suffer from laziness could be treated with medicine that targets the genes that specifically promote activity.
Scientists from the University of California found that on laboratory mice activity levels could be enhanced by selective breeding – the process of breeding animals for particular genetic traits.
Their study showed that mice bred to enjoy running produce offspring that also like it, showing that the baby mice had inherited the trait of high activity.
Professor Theodore Garland Jr, a biologist and lead author, said: "Our findings have implications for human health...
Conversely, the same is true about being a couch potato.
In the future, people who suffer from laziness could be treated with medicine that targets the genes that specifically promote activity.
Scientists from the University of California found that on laboratory mice activity levels could be enhanced by selective breeding – the process of breeding animals for particular genetic traits.
Their study showed that mice bred to enjoy running produce offspring that also like it, showing that the baby mice had inherited the trait of high activity.
Professor Theodore Garland Jr, a biologist and lead author, said: "Our findings have implications for human health...
Monday, August 30, 2010
Why men and women gain weight in different areas of the body
Why is it that men and women put on those extra kilos in different areas of the body? The answer may not be far away as researchers are close to revealing vital sex differences in men and women concerning fat storage.
The research has indicated that fat is genetically different in men and women.
"Given the difference in gene expression profiles, a female fat tissue won't behave anything like a male fat tissue and vice versa," said Deborah Clegg, of the UT Southwestern Medical Center.
"The notion that fat cells between males and females are alike is inconsistent with our findings," he said.
Mice store their fat similar to humans in a sexually dimorphic pattern. Just like human males, male mice store their fat in the belly and midsection area while females store fat in their hips, thighs and buttocks...
The research has indicated that fat is genetically different in men and women.
"Given the difference in gene expression profiles, a female fat tissue won't behave anything like a male fat tissue and vice versa," said Deborah Clegg, of the UT Southwestern Medical Center.
"The notion that fat cells between males and females are alike is inconsistent with our findings," he said.
Mice store their fat similar to humans in a sexually dimorphic pattern. Just like human males, male mice store their fat in the belly and midsection area while females store fat in their hips, thighs and buttocks...
Exercise 'can control appetite'
Exercise not only burns off calories, it can reduce feelings of hunger, scientists have said.
The findings suggest a "double whammy" benefit that may help the overweight to slim.
Researchers studying obese mice found that exercise restored the sensitivity of brain cells involved in controlling appetite.
The change increased satiety - or "feeling full" - in the animals and led to a reduction in food intake...
The findings suggest a "double whammy" benefit that may help the overweight to slim.
Researchers studying obese mice found that exercise restored the sensitivity of brain cells involved in controlling appetite.
The change increased satiety - or "feeling full" - in the animals and led to a reduction in food intake...
Saturday, August 21, 2010
Novel Diabetes Hope Comes from Chinese Herbs
Emodin, a natural product that can be extracted from various Chinese herbs including Rheum palmatum and Polygonum cuspidatum, shows promise as an agent that could reduce the impact of type 2 diabetes. Findings published in this month's edition of the British Journal of Pharmacology show that giving emodin to mice with diet-induced obesity lowered blood glucose and serum insulin, improved insulin resistance and lead to more healthy levels of lipid in the blood. It also decreased body weight and reduced central fat mass..
Thursday, August 12, 2010
Wouldn’t it be Great if You Could Pop a Pill and Lose Weight?
And wouldn't it be great if that pill weren't something advertised on late-night TV, but rather a legitimate treatment? A drug called rimonabant, introduced in Europe, seemed to fit the bill at first, but it was pulled from the market in late 2008 due to concerns about psychiatric side effects.
The story doesn't end there, though. New research on animals suggests that a second generation of drugs may treat obesity without those side effects. A presentation at the International Congress on Obesity in Stockholm, Sweden, revealed a treatment that has the same weight-loss effect as rimonabant, but without impacting the brain.
What's different? The new drug, currently called TM38837, does not affect peripheral organs and tissues. Rimonabant, however, didn't discriminate. According to earlier research, rimonabant doubled the risk of disorders such as depression and suicide.
In their new work, scientists tried the second-generation drug on mice and rats. After a five-week course of treatment, the mice had lost 22 to 26 percent more weight than mice in a control group. The rats had lost 14 percent more than the controls. In both cases, weight loss from TM38837 was the same as weight loss from rimonabant. Separate studies, including dissections and behavioral tests, showed that the drug was less likely to impact the brains of test animals...
The story doesn't end there, though. New research on animals suggests that a second generation of drugs may treat obesity without those side effects. A presentation at the International Congress on Obesity in Stockholm, Sweden, revealed a treatment that has the same weight-loss effect as rimonabant, but without impacting the brain.
What's different? The new drug, currently called TM38837, does not affect peripheral organs and tissues. Rimonabant, however, didn't discriminate. According to earlier research, rimonabant doubled the risk of disorders such as depression and suicide.
In their new work, scientists tried the second-generation drug on mice and rats. After a five-week course of treatment, the mice had lost 22 to 26 percent more weight than mice in a control group. The rats had lost 14 percent more than the controls. In both cases, weight loss from TM38837 was the same as weight loss from rimonabant. Separate studies, including dissections and behavioral tests, showed that the drug was less likely to impact the brains of test animals...
Sunday, August 08, 2010
Light Shed on Triglyceride Metabolism
New findings reported in the July issue of Cell Metabolism, are offering new leads as to why some people might suffer from high levels of triglycerides. High triglycerides are a risk factor for atherosclerosis and cardiovascular disease. They can also lead to inflammation of the pancreas, the researchers said...
It seems that a protein known as GPIHBP1 is the key. Mice lacking that protein end up with LPL built up outside of their muscle and fat tissue instead of where it belongs in capillaries. They show that GPIHBP1 normally sits on the surface of capillary cells, where it actively transports LPL.
The new findings offer an explanation for what had been a surprising finding; Gpihbp1-deficient mice develop severe hypertriglyceridemia, even when they eat a normal diet of mouse chow. Very recently, other researchers have also shown that some people with elevated triglyceride levels carry mutations in their GPIHBP1 gene...
It seems that a protein known as GPIHBP1 is the key. Mice lacking that protein end up with LPL built up outside of their muscle and fat tissue instead of where it belongs in capillaries. They show that GPIHBP1 normally sits on the surface of capillary cells, where it actively transports LPL.
The new findings offer an explanation for what had been a surprising finding; Gpihbp1-deficient mice develop severe hypertriglyceridemia, even when they eat a normal diet of mouse chow. Very recently, other researchers have also shown that some people with elevated triglyceride levels carry mutations in their GPIHBP1 gene...
Saturday, August 07, 2010
Calling all Obelixes! Hope at home - Indian researchers join global scramble to develop anti-obesity pill
New Delhi, July 31: A team of industry researchers in India has synthesised novel compounds that interfere with weight-gaining mechanisms in the body and joined an international scramble to develop a new class of anti-obesity pills.
The team at Dr Reddy’s Laboratories (DRL), Hyderabad, has shown in laboratory studies that one of these compounds, code-named 22g, helped gluttonous and obese mice lose 8 per cent of their body weight after seven days of oral medication...
The team at Dr Reddy’s Laboratories (DRL), Hyderabad, has shown in laboratory studies that one of these compounds, code-named 22g, helped gluttonous and obese mice lose 8 per cent of their body weight after seven days of oral medication...
ew loci for blood lipids identified; functional role of 1p13 locus detailed
Bethesda, MD and Boston, MA - Two new studies published this week provide further insights into the genetic underpinnings of variations in blood lipid levels [1,2]. In one large-scale genomewide association study (GWAS), researchers identified 95 loci that showed associations with blood lipid levels, while another group performed a detailed functional genomics analysis showing how a locus on chromosome 1p13, previously associated with low LDL-cholesterol levels and MI, regulates LDL-cholesterol levels.
"The two papers are highly complementary," Dr Sekar Kathiresan (Massachusetts General Hospital, Boston), a senior investigator of both studies, told heartwire. "The reason they're so complementary is that the first paper, the GWAS paper, puts down 95 stakes in the sand, while the second paper drills down on one of those stakes. We think the mapping effort, the GWAS paper, is incredibly important simply based on the scale of the effort. It's safe to say it's the largest genetics study done to date, and these 95 loci explain about 25% of the genetic component for lipid levels, which is among the largest proportion of variation evaluated to date."
The two studies are published in the August 5, 2010 issue of Nature...
To show that SORT1 is the causal gene, the researchers manipulated the gene in mice. With small interfering RNA "knockdown" and "viral overexpression" in the mouse liver, the researchers showed that the upregulation of SORT1 led to significantly lower LDL-cholesterol levels, as much as 80% lower, and that silencing SORT1 increased LDL cholesterol approximately 200%.
"Using these experiments in mice, we were able to prove that sortilin is the right gene for the LDL effect at the chromosome 1 locus," Kathiresan told heartwire. "And then, finally, if sortilin is the right gene, how does sortilin lower LDL cholesterol? We showed that the physiologic mechanism is that higher levels of sortilin lead to less secretion of very low-density lipoprotein (vLDL) from the liver, and vLDL is the precursor to LDL. Having less of the precursor around leads to less LDL, and this was the final piece of the puzzle."...
"The two papers are highly complementary," Dr Sekar Kathiresan (Massachusetts General Hospital, Boston), a senior investigator of both studies, told heartwire. "The reason they're so complementary is that the first paper, the GWAS paper, puts down 95 stakes in the sand, while the second paper drills down on one of those stakes. We think the mapping effort, the GWAS paper, is incredibly important simply based on the scale of the effort. It's safe to say it's the largest genetics study done to date, and these 95 loci explain about 25% of the genetic component for lipid levels, which is among the largest proportion of variation evaluated to date."
The two studies are published in the August 5, 2010 issue of Nature...
To show that SORT1 is the causal gene, the researchers manipulated the gene in mice. With small interfering RNA "knockdown" and "viral overexpression" in the mouse liver, the researchers showed that the upregulation of SORT1 led to significantly lower LDL-cholesterol levels, as much as 80% lower, and that silencing SORT1 increased LDL cholesterol approximately 200%.
"Using these experiments in mice, we were able to prove that sortilin is the right gene for the LDL effect at the chromosome 1 locus," Kathiresan told heartwire. "And then, finally, if sortilin is the right gene, how does sortilin lower LDL cholesterol? We showed that the physiologic mechanism is that higher levels of sortilin lead to less secretion of very low-density lipoprotein (vLDL) from the liver, and vLDL is the precursor to LDL. Having less of the precursor around leads to less LDL, and this was the final piece of the puzzle."...
All-Nighters May Increase Fat Levels in Blood
Disruptions to a person's normal sleep cycle, such as pulling several all-nighters, could lead to an increase in harmful triglycerides in the blood, a new study on mice suggests.
Though further studies are needed to firm up whether the same holds for humans, scientists often use these rodents as models for human systems.
The new findings could have implications for understanding the health effects of night shifts, 14-hour work days and transoceanic flights. High levels of triglycerides in the blood are a risk factor for heart disease and obesity – not only in mice, but also potentially in people, the researchers say...
Though further studies are needed to firm up whether the same holds for humans, scientists often use these rodents as models for human systems.
The new findings could have implications for understanding the health effects of night shifts, 14-hour work days and transoceanic flights. High levels of triglycerides in the blood are a risk factor for heart disease and obesity – not only in mice, but also potentially in people, the researchers say...
Insufficient ALA could be linked to obesity trend
A new study suggests that a deficiency in alpha-linoleic acid (omega-3) coupled with a chronic excess of linoleic acid (omega-6) could lead to ‘inherited obesity’.
The study, published in the Journal of Lipid Research, describes an increase in fat mass of mice over several generations when fed an ‘unbalanced Western diet’.
In addition to trans-generational weight gain, the research also observed the onset of metabolic disorders such as insulin resistance, and the expression of the inflammatory genes involved in obesity as generations advanced.
“Collectively, our data show that continuous exposure to a high-fat diet combined with a high LA:LNA [omega-6:omega-3] ratio over generations triggers a discrete and steady increase in inflammatory stimuli, accompanied by enhancement of fat mass” wrote the researchers.
Unbalanced Intake
The beneficial role that polyunsaturated fatty acids can have on health is well established. However when their intake is unbalanced, these essential fatty acids can enhance factors that can induce obesity, and may have serious long-term effects on human health.
During the last forty years Western societies have seen increases in the level of calories ingested, alongside an increase of over 250 percent in levels omega-6 intake and a fall in levels of omega-3 of 40 percent. This change in diet has coincided with a steady rise in obesity levels through the generations.
Over this time the ratio of omega-6 to omega-3 in a typical Western diet has shifted from the recommended 5-to-1, to 15-to-1 in much of Europe, and can be as high as 40-to-1 in the United States.
Alpha-linoleic acid (ALA) omega-3 is an essential fatty acid that the body cannot make, and therefore must be consumed in the diet. Good sources of ALA include: flaxseed, soybeans, walnuts, and olive oil. The U.S Institute of Medicine recommends an ALA intake of 1.6 grams per day for men and 1.1 grams per day for women.
Assessing the consequences
The new research, led by Gérard Ailhaud at the Université de Nice Sophia-Antipolis in France, exposed several generations of mice to a high omega-6 and low omega-3 "Western" diet and assessed the consequences.
The mice were given unrestricted access to food and water (ad libitum conditions) over several generations in order to allow the mice to self-regulate the intake according to biological needs.
“We chose purposely ad libitum conditions to expose both male and female mice across several generations to a Western-like diet” the researchers explain.
Trans-generational inheritance
The results of the study observe that under conditions of genetic stability and with no change to routine, four generations of a ‘Western-like fat diet’ were sufficient to gradually increase fat mass.
“A gradual trans-generational increase in adiposity can occur in mice fed a Western-like fat diet” wrote the researchers.
The study suggests that an unbalanced diet can lead to changes in the expression of genes that control growth and immune functions.
A gene expression analysis of fat tissue over several generations of the mice observed “discrete and steady changes in certain important players, such as colony stimulating factor-3 (CSF3) and Nocturnin.”
The researchers said “Our data show that expression of CSF-3 increased over generations in mice. These results strongly suggest a role for CSF-3 in stimulating growth of adipocyte progenitors.”...
The study, published in the Journal of Lipid Research, describes an increase in fat mass of mice over several generations when fed an ‘unbalanced Western diet’.
In addition to trans-generational weight gain, the research also observed the onset of metabolic disorders such as insulin resistance, and the expression of the inflammatory genes involved in obesity as generations advanced.
“Collectively, our data show that continuous exposure to a high-fat diet combined with a high LA:LNA [omega-6:omega-3] ratio over generations triggers a discrete and steady increase in inflammatory stimuli, accompanied by enhancement of fat mass” wrote the researchers.
Unbalanced Intake
The beneficial role that polyunsaturated fatty acids can have on health is well established. However when their intake is unbalanced, these essential fatty acids can enhance factors that can induce obesity, and may have serious long-term effects on human health.
During the last forty years Western societies have seen increases in the level of calories ingested, alongside an increase of over 250 percent in levels omega-6 intake and a fall in levels of omega-3 of 40 percent. This change in diet has coincided with a steady rise in obesity levels through the generations.
Over this time the ratio of omega-6 to omega-3 in a typical Western diet has shifted from the recommended 5-to-1, to 15-to-1 in much of Europe, and can be as high as 40-to-1 in the United States.
Alpha-linoleic acid (ALA) omega-3 is an essential fatty acid that the body cannot make, and therefore must be consumed in the diet. Good sources of ALA include: flaxseed, soybeans, walnuts, and olive oil. The U.S Institute of Medicine recommends an ALA intake of 1.6 grams per day for men and 1.1 grams per day for women.
Assessing the consequences
The new research, led by Gérard Ailhaud at the Université de Nice Sophia-Antipolis in France, exposed several generations of mice to a high omega-6 and low omega-3 "Western" diet and assessed the consequences.
The mice were given unrestricted access to food and water (ad libitum conditions) over several generations in order to allow the mice to self-regulate the intake according to biological needs.
“We chose purposely ad libitum conditions to expose both male and female mice across several generations to a Western-like diet” the researchers explain.
Trans-generational inheritance
The results of the study observe that under conditions of genetic stability and with no change to routine, four generations of a ‘Western-like fat diet’ were sufficient to gradually increase fat mass.
“A gradual trans-generational increase in adiposity can occur in mice fed a Western-like fat diet” wrote the researchers.
The study suggests that an unbalanced diet can lead to changes in the expression of genes that control growth and immune functions.
A gene expression analysis of fat tissue over several generations of the mice observed “discrete and steady changes in certain important players, such as colony stimulating factor-3 (CSF3) and Nocturnin.”
The researchers said “Our data show that expression of CSF-3 increased over generations in mice. These results strongly suggest a role for CSF-3 in stimulating growth of adipocyte progenitors.”...
Tuesday, July 27, 2010
Meals as Medicine: Anti-Obesity Effects of Soy in Rat Model of Menopause
Research presented at the Annual Meeting of the Society for the Study of Ingestive Behavior, finds that a diet rich in soy prevents weight gain in post-menopausal female rats.
Previous research suggests that reduced levels of the hormone estrogen during menopause are responsible for the increased body weight and abdominal fat often experienced by postmenopausal women. However, while estrogen replacement therapies can reduce weight gain, they also have unwelcome side effects, prompting a search for alternative methods of treatment. Soy naturally contains estrogen-like compounds called phytoestrogens, and so dietary soy may provide an alternative to typical estrogen replacement therapies...
Previous research suggests that reduced levels of the hormone estrogen during menopause are responsible for the increased body weight and abdominal fat often experienced by postmenopausal women. However, while estrogen replacement therapies can reduce weight gain, they also have unwelcome side effects, prompting a search for alternative methods of treatment. Soy naturally contains estrogen-like compounds called phytoestrogens, and so dietary soy may provide an alternative to typical estrogen replacement therapies...
Monday, July 26, 2010
New obesity compound shows promise in mice
A compound similar to the once-promising weight loss drug Acomplia helped obese mice lose weight and lower their blood fats and blood sugar without causing psychological side effects, U.S. researchers said on Monday.
Like Acomplia, the drug targets cannabinoid receptors that become active after smoking marijuana, but the team tinkered with the compound to keep it from crossing over into the brain, reducing the risk of depression, anxiety or other neurological problems seen in the original drug.
While obese mice do not lose as much weight on this new compound, it was just as effective as Acomplia in reducing obesity-related metabolic changes, researchers from the National Institutes of Health and Northeastern University reported in the Journal of Clinical Investigation...
Like Acomplia, the drug targets cannabinoid receptors that become active after smoking marijuana, but the team tinkered with the compound to keep it from crossing over into the brain, reducing the risk of depression, anxiety or other neurological problems seen in the original drug.
While obese mice do not lose as much weight on this new compound, it was just as effective as Acomplia in reducing obesity-related metabolic changes, researchers from the National Institutes of Health and Northeastern University reported in the Journal of Clinical Investigation...
Sunday, July 25, 2010
Resveratrol revs up metabolism, promotes weight loss in first ever primate study
Resveratrol is a type of phytonutrient known as a polyphenol. Found in the skin of grapes, wine, grape juice, peanuts, and berries, it has often been hailed as a life-extending natural compound. After all, research in mice and lab rats has indicated it can protect those animals from obesity and diabetes and has anti-cancer, anti-inflammatory and blood-sugar-lowering effects, too. However, rats and mice are rodents -- and their physiology is in many ways different from the primate family that includes apes, monkeys and, most importantly, human beings...
Scientists find unsuspected molecular link between obesity and insulin resistance
A new understanding of insulin resistance and the action of diabetes drugs such as Avandia and Actos could pave the way for improved medications that are more selective and safer, say scientists from Dana-Farber Cancer Institute and The Scripps Research Institute.
Our findings strongly suggest that good and bad effects of these drugs can be separated by designing second-generation drugs that focus on the newly uncovered mechanism, said Bruce Spiegelman, PhD, of Dana-Farber, senior author on a report appearing in the July 22 issue of Nature.
Avandia and Actos, known generically as rosiglitazone and pioglitazone, are widely used to counteract the obesity-related abnormalities in insulin response that lead to diabetes. The drugs act on a master regulatory protein called PPAR-gamma, primarily in fat cells, which governs genes involved in the bodys response to insulin.
Obesity resulting from a high-fat diet alters the function of PPAR-gamma and disrupts the expression of those insulin response genes, including adipsin and adiponectin. Avandia and Actos work by binding to PPAR-gamma and reversing the gene expression changes.
The drugs were believed to work by stimulating or agonizing the PPAR-gamma receptor, causing it to rev up some genes and dampen the activity of others.
In the Nature report, however, the researchers say they have identified an entirely new and surprising mechanism by which PPAR-gamma can control whole-body insulin sensitivity. It is mainly through this mechanism, they found, that the diabetes drugs counteract insulin resistance – not their agonist effect on PPAR-gamma. Moreover, they say, agonism of PPAR-gamma may be largely responsible for the harmful drug side effects.
The newly identified pathway linking obesity and insulin response involves cdk5, a protein kinase, or molecular switch. When cdk5 is activated by the development of obesity in mice, it causes a chemical change in PPAR-gamma called phosphorylation. In contrast to agonism of PPAR-gamma, phosphorylation has a narrow effect, disrupting a smaller set of genes that lead to insulin resistance...
Our findings strongly suggest that good and bad effects of these drugs can be separated by designing second-generation drugs that focus on the newly uncovered mechanism, said Bruce Spiegelman, PhD, of Dana-Farber, senior author on a report appearing in the July 22 issue of Nature.
Avandia and Actos, known generically as rosiglitazone and pioglitazone, are widely used to counteract the obesity-related abnormalities in insulin response that lead to diabetes. The drugs act on a master regulatory protein called PPAR-gamma, primarily in fat cells, which governs genes involved in the bodys response to insulin.
Obesity resulting from a high-fat diet alters the function of PPAR-gamma and disrupts the expression of those insulin response genes, including adipsin and adiponectin. Avandia and Actos work by binding to PPAR-gamma and reversing the gene expression changes.
The drugs were believed to work by stimulating or agonizing the PPAR-gamma receptor, causing it to rev up some genes and dampen the activity of others.
In the Nature report, however, the researchers say they have identified an entirely new and surprising mechanism by which PPAR-gamma can control whole-body insulin sensitivity. It is mainly through this mechanism, they found, that the diabetes drugs counteract insulin resistance – not their agonist effect on PPAR-gamma. Moreover, they say, agonism of PPAR-gamma may be largely responsible for the harmful drug side effects.
The newly identified pathway linking obesity and insulin response involves cdk5, a protein kinase, or molecular switch. When cdk5 is activated by the development of obesity in mice, it causes a chemical change in PPAR-gamma called phosphorylation. In contrast to agonism of PPAR-gamma, phosphorylation has a narrow effect, disrupting a smaller set of genes that lead to insulin resistance...
Lose sleep, get fat?
LOS ANGELES — Disrupted sleep patterns seem to contribute to the risk of obesity and diabetes, according to numerous studies. Researchers have theorized that disrupted circadian rhythms throw off various hormonal processes in the body that contribute to disease.
This theory is looking stronger all the time, and the mounting evidence bolsters the argument that people should care about their sleep habits. Researchers at University of Texas Southwestern Medical Center in Dallas have found that mice with defective copies of two genes involved in circadian rhythms develop abnormalities in their pancreatic cells that eventually cause problems with the release of insulin.
One gene, the CLOCK gene, operates in many parts of the body to control circadian processes. The other gene, BMAL1, works with the CLOCK protein. In the study, scientists engineered some mice to have defective CLOCK genes in the pancreas and some to lack the BMAL1 gene. They found that mice with the mutant CLOCK gene were defective in releasing insulin. These mice were prone to obesity and other health problems related to liver and metabolic function. The mice lacking the BMAL1 gene in their pancreas had normal body weight and normal circadian patterns but had abnormal blood sugar levels.
The study shows that disruption of these genes only in the pancreas causes early signs of diabetes...
This theory is looking stronger all the time, and the mounting evidence bolsters the argument that people should care about their sleep habits. Researchers at University of Texas Southwestern Medical Center in Dallas have found that mice with defective copies of two genes involved in circadian rhythms develop abnormalities in their pancreatic cells that eventually cause problems with the release of insulin.
One gene, the CLOCK gene, operates in many parts of the body to control circadian processes. The other gene, BMAL1, works with the CLOCK protein. In the study, scientists engineered some mice to have defective CLOCK genes in the pancreas and some to lack the BMAL1 gene. They found that mice with the mutant CLOCK gene were defective in releasing insulin. These mice were prone to obesity and other health problems related to liver and metabolic function. The mice lacking the BMAL1 gene in their pancreas had normal body weight and normal circadian patterns but had abnormal blood sugar levels.
The study shows that disruption of these genes only in the pancreas causes early signs of diabetes...
AMRI Announces Phase I Study of Novel Drug for Obesity Treatment
ALBANY, N.Y., Jul 21, 2010 (BUSINESS WIRE) -- AMRI (AMRI 6.86, +0.34, +5.21%) has commenced enrollment for a Phase I study of ALB-127158(a), a novel MCH1 receptor antagonist offering a potential new approach for the treatment of obesity. The announcement was made yesterday during a presentation by AMRI's Dr. Peter Guzzo, director, discovery research and development, at the 6th Obesity and Diabetes Drug Development Summit in Arlington, VA. Preclinical data were also reported.
The clinical trial will be comprised of a single ascending dose study followed by a multiple ascending dose study to assess safety, tolerability and pharmacokinetics. The multiple ascending dose study will be conducted in overweight subjects to evaluate pharmacodynamics (the physiological effects of the drug candidate on the body), including caloric intake, hunger assessments and metabolic markers. The Phase I study is anticipated to be completed during the first quarter of 2011.
Preclinical studies of the AMRI compound have suggested promise for the treatment of human obesity. For example, in data presented by Dr. Guzzo, ALB-127158(a) showed high levels of MCH1 receptor occupancy leading to a sustained, dose-related reduction in food intake in dietary-induced obese mice. The ensuing weight loss of up to 18% after 28 days of administration was substantially higher than that from the currently available therapeutic agent, sibutramine. Weight loss was shown to be entirely due to a reduction in food intake leading to a preferential reduction in fat stores and was accompanied by significant improvements in glucose tolerance. Preliminary safety evaluation, including cardiovascular safety, was also reported; subsequent regulatory safety testing supported approval by the UK Medicines and Healthcare Products Regulatory Agency for initiation of the Phase I study...
The clinical trial will be comprised of a single ascending dose study followed by a multiple ascending dose study to assess safety, tolerability and pharmacokinetics. The multiple ascending dose study will be conducted in overweight subjects to evaluate pharmacodynamics (the physiological effects of the drug candidate on the body), including caloric intake, hunger assessments and metabolic markers. The Phase I study is anticipated to be completed during the first quarter of 2011.
Preclinical studies of the AMRI compound have suggested promise for the treatment of human obesity. For example, in data presented by Dr. Guzzo, ALB-127158(a) showed high levels of MCH1 receptor occupancy leading to a sustained, dose-related reduction in food intake in dietary-induced obese mice. The ensuing weight loss of up to 18% after 28 days of administration was substantially higher than that from the currently available therapeutic agent, sibutramine. Weight loss was shown to be entirely due to a reduction in food intake leading to a preferential reduction in fat stores and was accompanied by significant improvements in glucose tolerance. Preliminary safety evaluation, including cardiovascular safety, was also reported; subsequent regulatory safety testing supported approval by the UK Medicines and Healthcare Products Regulatory Agency for initiation of the Phase I study...
Good news for Obese people
WASHINGTON: Researchers at Washington University School of Medicine in St Louis have found a way to significantly reduce atherosclerosis in mice without lowering cholesterol levels or eliminating other obesity-related problems.
Atherosclerosis is the process through which fatty substances, such as cholesterol and cellular waste products accumulate in the lining of arteries.
Those buildups, called plaques, reduce blood flow through the artery and can contribute to heart attack, stroke and even gangrene. It is common in individuals with obesity-related problems such as high blood pressure, high cholesterol and diabetes.
In the study, researchers inhibited atherosclerosis in mice by interfering with production of a substance called fatty acid synthase.
This enzyme converts dietary sugars into fatty acids in the liver, where it plays an important role in energy metabolism.
But fatty acids also are involved in atherosclerosis.
"The plaques that clog arteries contain large amounts of fatty acids. We engineered mice that are unable to make fatty acid synthase in one of the major cell types that contribute to plaque formation. On a standard Western diet high in fat, the mice had less atherosclerosis than their normal littermates," said senior investigator Dr. Clay F. Semenkovich.
Animals can't survive without fatty acid synthase, so mice in this study were able to make the substance in most of their tissues.
They couldn't manufacture it, however, in macrophages, a type of white blood cell that surrounds and kills invading microorganisms, removes dead cells from the body and stimulates the action of other immune cells.
These mouse experiments suggest targeting fatty acid synthase in macrophages may provide a potential treatment strategy for humans.
The researchers identified factors in the fatty acid pathway that seem to be capable of preventing plaques from blocking arteries in mice.
He says those substances - LXR-alpha and ABCA1 - eventually may become drug targets.
"It may be possible, for example, to take macrophages out of humans, inhibit fatty acid synthase in those cells, and then infuse the macrophages back into the same personFrom what we've observed in mice, we would hypothesize that approach might prevent or interfere with plaque buildup in people," he said...
Atherosclerosis is the process through which fatty substances, such as cholesterol and cellular waste products accumulate in the lining of arteries.
Those buildups, called plaques, reduce blood flow through the artery and can contribute to heart attack, stroke and even gangrene. It is common in individuals with obesity-related problems such as high blood pressure, high cholesterol and diabetes.
In the study, researchers inhibited atherosclerosis in mice by interfering with production of a substance called fatty acid synthase.
This enzyme converts dietary sugars into fatty acids in the liver, where it plays an important role in energy metabolism.
But fatty acids also are involved in atherosclerosis.
"The plaques that clog arteries contain large amounts of fatty acids. We engineered mice that are unable to make fatty acid synthase in one of the major cell types that contribute to plaque formation. On a standard Western diet high in fat, the mice had less atherosclerosis than their normal littermates," said senior investigator Dr. Clay F. Semenkovich.
Animals can't survive without fatty acid synthase, so mice in this study were able to make the substance in most of their tissues.
They couldn't manufacture it, however, in macrophages, a type of white blood cell that surrounds and kills invading microorganisms, removes dead cells from the body and stimulates the action of other immune cells.
These mouse experiments suggest targeting fatty acid synthase in macrophages may provide a potential treatment strategy for humans.
The researchers identified factors in the fatty acid pathway that seem to be capable of preventing plaques from blocking arteries in mice.
He says those substances - LXR-alpha and ABCA1 - eventually may become drug targets.
"It may be possible, for example, to take macrophages out of humans, inhibit fatty acid synthase in those cells, and then infuse the macrophages back into the same personFrom what we've observed in mice, we would hypothesize that approach might prevent or interfere with plaque buildup in people," he said...
Chokeberry Extract Found to Regulate Weight Gain, Blood Glucose, and Inflammation in Rats
Chokeberry bushes have for centuries been residents of eastern deciduous forests where their bright red and dark purple fruits continue to be favorite snacks of local bird species. Native Americans have also traditionally eaten dried chokeberries and prepared teas from parts of the plant, and several domesticated varieties now grace contemporary lawns and gardens from coast to coast. However, the chokeberry (Aronia) is enjoying a new claim-to-fame as a potentially powerful antioxidant, and can now be found for sale in the dietary supplement and "health food" aisles of your local pharmacies and grocery stores.
What makes the humble chokeberry so healthful? Scientists think the answer lies in their unusually high levels of substances called anthocyanins (from the Greek anthos + kyanos meaning dark blue). There are many different anthocyanins in these colorful berries, but they all function as antioxidants -- originally protecting the chokeberry seed from sunshine-induced oxidative stress. And when we eat them, they also appear to protect our bodies from a variety of damaging situations, including exposure to pollution and metabolically-derived free radicals. Indeed, a growing body of scientific literature has shown promising effects of chokeberry consumption on diseases ranging from cancer to obesity. These health-promoting effects may be due to the potent anti-inflammatory properties of anthocyanins, as uncontrolled inflammation is now universally recognized as a common thread in many of our most prevalent and deadly diseases. In addition, certain anthocyanins -- including those found in chokeberry -- have also been shown to improve blood sugar and the function of insulin.
To better understand how chokeberries influence health, Drs. Bolin Qin and Richard Anderson from the US Department of Agriculture in Beltsville, MD studied what happens when prediabetic rats are fed chokeberry extracts for an extended period of time. The results of their research were presented on April 25 at the Experimental Biology 2010 meeting in Anaheim, CA. This presentation is part of the scientific program of the American Society for Nutrition, home of the world's leading nutrition researchers.
The researchers first made 18 male rats "prediabetic" or insulin insensitive by feeding them a fructose-rich diet for 6 weeks. Then they randomized the animals to continue drinking either pure water or water spiked with low or high levels of chokeberry extract (CellBerry®, Integrity Nutraceuticals International). After drinking this water for 6 weeks, the groups were compared in terms of body weight, body fat, blood glucose regulation, and molecular markers for inflammation.
Qin and Anderson found that at the end of the study the rats consuming the chokeberry-spiked water weighed less than the controls; both levels of chokeberry had the same effect in this regard. Similar beneficial effects of chokeberry consumption were found for body fat (specifically, that of the lower abdominal region). They also discovered that animals that had been drinking chokeberry extract had lower blood glucose and reduced levels of plasma triglycerides, cholesterol, and low-density lipoprotein (LDL) cholesterol when compared to the control animals. These alterations would theoretically lead to lower risk for diabetes and cardiovascular disease in humans. And to add even more evidence for a healthful impact of this super-berry, the researchers documented numerous alterations in expression of genes that would likely lead to reduced chronic inflammation and perhaps even lower cancer risk. For instance, drinking chokeberry extract lowered expression of the gene coding for interleukin-6 (IL-6), a protein that normally triggers inflammation following trauma or infection. Chronic overproduction of IL-6 has been documented in many diseases such as diabetes, arthritis, and atherosclerosis and is thought to be a partial cause of these conditions.
Of course, human studies will be needed before scientists can declare whether we derive the same health benefits from the chokeberry...
What makes the humble chokeberry so healthful? Scientists think the answer lies in their unusually high levels of substances called anthocyanins (from the Greek anthos + kyanos meaning dark blue). There are many different anthocyanins in these colorful berries, but they all function as antioxidants -- originally protecting the chokeberry seed from sunshine-induced oxidative stress. And when we eat them, they also appear to protect our bodies from a variety of damaging situations, including exposure to pollution and metabolically-derived free radicals. Indeed, a growing body of scientific literature has shown promising effects of chokeberry consumption on diseases ranging from cancer to obesity. These health-promoting effects may be due to the potent anti-inflammatory properties of anthocyanins, as uncontrolled inflammation is now universally recognized as a common thread in many of our most prevalent and deadly diseases. In addition, certain anthocyanins -- including those found in chokeberry -- have also been shown to improve blood sugar and the function of insulin.
To better understand how chokeberries influence health, Drs. Bolin Qin and Richard Anderson from the US Department of Agriculture in Beltsville, MD studied what happens when prediabetic rats are fed chokeberry extracts for an extended period of time. The results of their research were presented on April 25 at the Experimental Biology 2010 meeting in Anaheim, CA. This presentation is part of the scientific program of the American Society for Nutrition, home of the world's leading nutrition researchers.
The researchers first made 18 male rats "prediabetic" or insulin insensitive by feeding them a fructose-rich diet for 6 weeks. Then they randomized the animals to continue drinking either pure water or water spiked with low or high levels of chokeberry extract (CellBerry®, Integrity Nutraceuticals International). After drinking this water for 6 weeks, the groups were compared in terms of body weight, body fat, blood glucose regulation, and molecular markers for inflammation.
Qin and Anderson found that at the end of the study the rats consuming the chokeberry-spiked water weighed less than the controls; both levels of chokeberry had the same effect in this regard. Similar beneficial effects of chokeberry consumption were found for body fat (specifically, that of the lower abdominal region). They also discovered that animals that had been drinking chokeberry extract had lower blood glucose and reduced levels of plasma triglycerides, cholesterol, and low-density lipoprotein (LDL) cholesterol when compared to the control animals. These alterations would theoretically lead to lower risk for diabetes and cardiovascular disease in humans. And to add even more evidence for a healthful impact of this super-berry, the researchers documented numerous alterations in expression of genes that would likely lead to reduced chronic inflammation and perhaps even lower cancer risk. For instance, drinking chokeberry extract lowered expression of the gene coding for interleukin-6 (IL-6), a protein that normally triggers inflammation following trauma or infection. Chronic overproduction of IL-6 has been documented in many diseases such as diabetes, arthritis, and atherosclerosis and is thought to be a partial cause of these conditions.
Of course, human studies will be needed before scientists can declare whether we derive the same health benefits from the chokeberry...
Tuesday, July 20, 2010
Study Suggests Brown Adipose Tissue Involved in Increased Energy Expenditure after Capsinoids Ingestion
Ajinomoto Co., Inc. and a group led by professor Masayuki Saito of Tenshi College in Sapporo, Japan have found that a single ingestion of capsinoids, a sweet chili pepper extract, appears to increase energy expenditure, especially in people with a high level of activity in brown adipose tissue. The research results were presented at the XI International Congress on Obesity 2010 (ICO 2010) on July 13 in Stockholm, Sweden.
The finding may have implications for controlling obesity, which is affected by the activation of brown adipose tissue according to recent studies.
Previous research with animals such as mice has shown that brown adipose tissue is involved in the regulation of energy expenditure and changes in body-fat levels. Brown adipose tissue in humans and several types of animals is mainly located around the neck and large blood vessels of the thorax. Fat is broken down in the mitochondria of brown adipose tissue cells to generate body heat. Although brown adipose tissue exists to some degree in human infants, the once-conventional view was that the tissue gradually deteriorates and is barely detectable in adults, with virtually no physiological role. In recent years, however, the group led by professor Saito has used PET imaging1 to confirm that brown adipose tissue is present in adults...
The finding may have implications for controlling obesity, which is affected by the activation of brown adipose tissue according to recent studies.
Previous research with animals such as mice has shown that brown adipose tissue is involved in the regulation of energy expenditure and changes in body-fat levels. Brown adipose tissue in humans and several types of animals is mainly located around the neck and large blood vessels of the thorax. Fat is broken down in the mitochondria of brown adipose tissue cells to generate body heat. Although brown adipose tissue exists to some degree in human infants, the once-conventional view was that the tissue gradually deteriorates and is barely detectable in adults, with virtually no physiological role. In recent years, however, the group led by professor Saito has used PET imaging1 to confirm that brown adipose tissue is present in adults...
Omega imbalance can make obesity 'inheritable': study
Overeating combined with the wrong mix of fats in one's diet can cause obesity to be carried over from one generation to the next, researchers in France reported Friday.
Omega-6 and omega-3, both polyunsaturated fatty acids, are each critical to good health.
But too much of the first and not enough of the second can lead to overweight offspring, the scientists showed in experiments with mice designed to mirror recent shifts in human diet.
Over the last four decades, the ratio of omega-6 to omega-3 in a typical Western diet has shifted from a healthy five-to-one to 15-to-one in much of Europe, and up to 40-to-one in the United States.
In the breast milk of American women, the average ratio has gone from six-to-one to 18-to-one.
Earlier studies have established a link between such imbalances and heart disease.
But "this is the first time that we have shown a trans-generational increase in obesity" linked to omega intake, said Gerard Ailhaud, a biochemist at the University of Nice-Sophia Antipolis and main architect of the study.
"Omega six is like a fat-producing bomb," he told AFP by phone.
Experts differ on whether obesity is more importantly due to the percentage of fat in one's diet or the sheer amount of calories consumed.
The findings, published in the US-based Journal of Lipid Research, add yet another dimension to the debate, and could shed new light on the obesity epidemic that has swept across the globe, mainly in rich nations.
They also suggest that persistence within families of health-threatening weight gain -- while not genetic in origin -- may not be entirely due to environmental factors either.
The link between omega imbalance and obesity "is probably epigenetic," said Ailhaud, referring to the complex process whereby the information in genes is translated into chemical activity.
"The genome and the DNA of the rodents has not been modified, but these factors can influence the way in which certain genes are expressed."
In the experiments, four generations of mice were fed a 35-percent fat diet with the omega imbalance now found in much of the developed world.
The result was progressively fatter mice at birth, generation after generation...
Omega-6 and omega-3, both polyunsaturated fatty acids, are each critical to good health.
But too much of the first and not enough of the second can lead to overweight offspring, the scientists showed in experiments with mice designed to mirror recent shifts in human diet.
Over the last four decades, the ratio of omega-6 to omega-3 in a typical Western diet has shifted from a healthy five-to-one to 15-to-one in much of Europe, and up to 40-to-one in the United States.
In the breast milk of American women, the average ratio has gone from six-to-one to 18-to-one.
Earlier studies have established a link between such imbalances and heart disease.
But "this is the first time that we have shown a trans-generational increase in obesity" linked to omega intake, said Gerard Ailhaud, a biochemist at the University of Nice-Sophia Antipolis and main architect of the study.
"Omega six is like a fat-producing bomb," he told AFP by phone.
Experts differ on whether obesity is more importantly due to the percentage of fat in one's diet or the sheer amount of calories consumed.
The findings, published in the US-based Journal of Lipid Research, add yet another dimension to the debate, and could shed new light on the obesity epidemic that has swept across the globe, mainly in rich nations.
They also suggest that persistence within families of health-threatening weight gain -- while not genetic in origin -- may not be entirely due to environmental factors either.
The link between omega imbalance and obesity "is probably epigenetic," said Ailhaud, referring to the complex process whereby the information in genes is translated into chemical activity.
"The genome and the DNA of the rodents has not been modified, but these factors can influence the way in which certain genes are expressed."
In the experiments, four generations of mice were fed a 35-percent fat diet with the omega imbalance now found in much of the developed world.
The result was progressively fatter mice at birth, generation after generation...
Disrupted sleep patterns could add to risk of obesity, diabetes
Disrupted sleep patterns seem to contribute to the risk of obesity and diabetes, according to numerous studies. Researchers have theorized that disrupted circadian rhythms throw off various hormonal processes in the body that contribute to disease.
This theory is looking stronger all the time, and the mounting evidence bolsters the argument that people should care about their sleep habits. Researchers at UT Southwestern Medical Center in Dallas have found that mice with defective copies of two genes involved in circadian rhythms develop abnormalities in their pancreatic cells that eventually cause problems with the release of insulin.
One gene, the CLOCK gene, operates in many parts of the body to control circadian processes. The other gene, BMAL1, works with the CLOCK protein. In the study, scientists engineered some mice to have defective CLOCK genes in the pancreas and some to lack the BMAL1 gene. They found that mice with the mutant CLOCK gene were defective in releasing insulin. These mice were prone to obesity and other health problems related to liver and metabolic function. The mice lacking the BMAL1 gene in their pancreas had normal body weight and normal circadian patterns but had abnormal blood sugar levels...
This theory is looking stronger all the time, and the mounting evidence bolsters the argument that people should care about their sleep habits. Researchers at UT Southwestern Medical Center in Dallas have found that mice with defective copies of two genes involved in circadian rhythms develop abnormalities in their pancreatic cells that eventually cause problems with the release of insulin.
One gene, the CLOCK gene, operates in many parts of the body to control circadian processes. The other gene, BMAL1, works with the CLOCK protein. In the study, scientists engineered some mice to have defective CLOCK genes in the pancreas and some to lack the BMAL1 gene. They found that mice with the mutant CLOCK gene were defective in releasing insulin. These mice were prone to obesity and other health problems related to liver and metabolic function. The mice lacking the BMAL1 gene in their pancreas had normal body weight and normal circadian patterns but had abnormal blood sugar levels...
Thursday, July 15, 2010
Crucial Aspects Of Brain Dopamine Signaling Altered By A High Fat Diet
Research presented at the Annual Meeting of the Society for the Study of Ingestive Behavior (SSIB), the foremost society for research into all aspects of eating and drinking behavior, finds that prolonged exposure to a high fat diet is correlated with changes in the brain chemical dopamine within the striatum, a critical component of the brain's reward system.
The authors measured 'real-time' changes in dopamine levels after rats consumed a high fat diet for either 2 or 6 weeks. Compared to rats consuming a standard low fat diet, high-fat diet rats exhibited reduced dopamine release and also reduced reuptake by "dopamine transporters" within the striatum. Mitchell Roitman from the University of Illinois at Chicago says, "Previous research has demonstrated reduced dopamine transporter numbers in association with obesity and exposure to a high fat diet. Our research shows that these changes lead to major differences in the way dopamine functions in the brain." The results from this study highlight the impact of diet on brain neurochemistry - and in particular on brain systems that regulate motivation and willingness to work for food reward in rats as well as humans...
The authors measured 'real-time' changes in dopamine levels after rats consumed a high fat diet for either 2 or 6 weeks. Compared to rats consuming a standard low fat diet, high-fat diet rats exhibited reduced dopamine release and also reduced reuptake by "dopamine transporters" within the striatum. Mitchell Roitman from the University of Illinois at Chicago says, "Previous research has demonstrated reduced dopamine transporter numbers in association with obesity and exposure to a high fat diet. Our research shows that these changes lead to major differences in the way dopamine functions in the brain." The results from this study highlight the impact of diet on brain neurochemistry - and in particular on brain systems that regulate motivation and willingness to work for food reward in rats as well as humans...
New Research Finds That Chemicals In Soy Reduce Weight Gain In A Rat Model Of Menopause
Research presented at the Annual Meeting of the Society for the Study of Ingestive Behavior (SSIB), the foremost society for research into all aspects of eating and drinking behavior, finds that a diet rich in soy prevents weight gain in post-menopausal female rats...
Adiposity Hormone, Leptin, Regulates Food Intake By Influencing Learning And Memory
New animal research reveals mechanism that links memory and feeding behavior with leptin, a hormone released from fat cells
Research presented at the Annual Meeting of the Society for the Study of Ingestive Behavior (SSIB), the foremost society for research into all aspects of eating and drinking behavior, finds that the hormone leptin reduces food intake, in part, by activating the hippocampus, an area of the brain that controls learning and memory function. Leptin is a hormone released from fat cells that acts on the brain to inhibit feeding.
Researchers from the University of Pennsylvania found that when leptin was delivered directly to the hippocampus in rats, the animals consumed less food and lost body weight. Leptin delivered to this region of the brain also impaired the ability of the animals to learn about the spatial location of food...
Research presented at the Annual Meeting of the Society for the Study of Ingestive Behavior (SSIB), the foremost society for research into all aspects of eating and drinking behavior, finds that the hormone leptin reduces food intake, in part, by activating the hippocampus, an area of the brain that controls learning and memory function. Leptin is a hormone released from fat cells that acts on the brain to inhibit feeding.
Researchers from the University of Pennsylvania found that when leptin was delivered directly to the hippocampus in rats, the animals consumed less food and lost body weight. Leptin delivered to this region of the brain also impaired the ability of the animals to learn about the spatial location of food...
Greater Risk For Infant Obesity And Pre-Diabetes When Mothers Consumed A High Fat Diet While Nursing; But Not During Pregnancy
The future health of offspring is more negatively impacted when their mothers consume a high fat diet while nursing compared with high-fat diet consumption during pregnancy, according to animal research at Johns Hopkins University. These new research results were presented at the Annual Meeting of the Society for the Study of Ingestive Behavior (SSIB), the foremost society for research into all aspects of eating and drinking behavior.
The researchers used a method called "cross-fostering" to determine whether prenatal or postnatal exposure to maternal high fat diet has a greater influence on the development of obesity and diabetes in the offspring. Rats were fed either a low fat or high fat diet during pregnancy. After birth, pups born to mothers that consumed either diet were fostered over to different mother rats that ate the same or opposite diet during the nursing period. The researchers found that rat pups nursed by mothers consuming a high fat diet gained more body weight and were obese when weaned a few weeks later, even if the pup's biological mother ate a low fat diet during pregnancy. In addition to being obese, pups nursed by foster mothers on a high fat diet displayed impaired glucose tolerance, an early indicator of diabetes...
The researchers used a method called "cross-fostering" to determine whether prenatal or postnatal exposure to maternal high fat diet has a greater influence on the development of obesity and diabetes in the offspring. Rats were fed either a low fat or high fat diet during pregnancy. After birth, pups born to mothers that consumed either diet were fostered over to different mother rats that ate the same or opposite diet during the nursing period. The researchers found that rat pups nursed by mothers consuming a high fat diet gained more body weight and were obese when weaned a few weeks later, even if the pup's biological mother ate a low fat diet during pregnancy. In addition to being obese, pups nursed by foster mothers on a high fat diet displayed impaired glucose tolerance, an early indicator of diabetes...
Wednesday, July 14, 2010
Mice Essentially 'Cured' of Mild Diabetes With Enzyme
Nutrition experts at Oregon State University have essentially "cured" laboratory mice of mild, diet-induced diabetes by stimulating the production of a particular enzyme.
The findings could offer a new approach to diabetes therapy, experts say, especially if a drug could be identified that would do the same thing, which in this case was accomplished with genetic manipulation.
Increased levels of this enzyme, called fatty acid elongase-5, restored normal function to diseased livers in mice, restored normal levels of blood glucose and insulin, and effectively corrected the risk factors incurred with diet-induced diabetes.
"This effect was fairly remarkable and not anticipated," said Donald Jump, a professor of nutrition and exercise sciences at Oregon State, where he is an expert on lipid metabolism and principal investigator with OSU's Linus Pauling Institute.
"It doesn't provide a therapy yet, but could be fairly important if we can find a drug to raise levels of this enzyme," Jump said. "There are already some drugs on the market that do this to a point, and further research in the field would be merited."
The studies were done on a family of enzymes called "fatty acid elongases," which have been known of for decades. Humans get essential fatty acids that they cannot naturally make from certain foods in their diet. These essential fatty acids are converted to longer and more unsaturated fatty acids. The fatty acid end products of these reactions are important for managing metabolism, inflammation, cognitive function, cardiovascular health, reproduction, vision and other metabolic roles.
The enzymes that do this are called fatty acid elongases, and much has been learned in recent years about them. In research on diet-induced obesity and diabetes, OSU studied enzyme conversion pathways, and found that elongase-5 was often impaired in mice with elevated insulin levels and diet-induced obesity.
The scientists used an established system, based on a recombinant adenovirus, to import the gene responsible for production of elongase-5 into the livers of obese, diabetic mice. When this "delivery system" began to function and the mice produced higher levels of the enzyme, their diet-induced liver defects and elevated blood sugar disappeared.
"The use of a genetic delivery system such as this was functional, but it may not be a permanent solution," Jump said. "For human therapy, it would be better to find a drug that could accomplish the same thing, and that may be possible. There are already drugs on the market, such as some fibrate drugs, that induce higher levels of elongase-5 to some extent."
There are also drugs used with diabetic patients that can lower blood sugar levels, Jump said, but some have side effects and undesired complications. The potential for raising levels of elongase-5 would be a new, specific and targeted approach to diabetes therapy, he said. While lowering blood sugar, the elevated levels of elongase-5 also reduced triglycerides in the liver, another desirable goal. Elevated triglycerides are associated with "fatty liver," also known as non-alcoholic fatty liver disease. This can progress to more severe liver diseases such as fibrosis, cirrhosis and cancer.
Further research is needed to define the exact biological mechanisms at work in this process, and determine what the fatty acids do that affects carbohydrate and triglyceride metabolism, he said. It appears that high fat diets suppress elongase-5 activity...
The findings could offer a new approach to diabetes therapy, experts say, especially if a drug could be identified that would do the same thing, which in this case was accomplished with genetic manipulation.
Increased levels of this enzyme, called fatty acid elongase-5, restored normal function to diseased livers in mice, restored normal levels of blood glucose and insulin, and effectively corrected the risk factors incurred with diet-induced diabetes.
"This effect was fairly remarkable and not anticipated," said Donald Jump, a professor of nutrition and exercise sciences at Oregon State, where he is an expert on lipid metabolism and principal investigator with OSU's Linus Pauling Institute.
"It doesn't provide a therapy yet, but could be fairly important if we can find a drug to raise levels of this enzyme," Jump said. "There are already some drugs on the market that do this to a point, and further research in the field would be merited."
The studies were done on a family of enzymes called "fatty acid elongases," which have been known of for decades. Humans get essential fatty acids that they cannot naturally make from certain foods in their diet. These essential fatty acids are converted to longer and more unsaturated fatty acids. The fatty acid end products of these reactions are important for managing metabolism, inflammation, cognitive function, cardiovascular health, reproduction, vision and other metabolic roles.
The enzymes that do this are called fatty acid elongases, and much has been learned in recent years about them. In research on diet-induced obesity and diabetes, OSU studied enzyme conversion pathways, and found that elongase-5 was often impaired in mice with elevated insulin levels and diet-induced obesity.
The scientists used an established system, based on a recombinant adenovirus, to import the gene responsible for production of elongase-5 into the livers of obese, diabetic mice. When this "delivery system" began to function and the mice produced higher levels of the enzyme, their diet-induced liver defects and elevated blood sugar disappeared.
"The use of a genetic delivery system such as this was functional, but it may not be a permanent solution," Jump said. "For human therapy, it would be better to find a drug that could accomplish the same thing, and that may be possible. There are already drugs on the market, such as some fibrate drugs, that induce higher levels of elongase-5 to some extent."
There are also drugs used with diabetic patients that can lower blood sugar levels, Jump said, but some have side effects and undesired complications. The potential for raising levels of elongase-5 would be a new, specific and targeted approach to diabetes therapy, he said. While lowering blood sugar, the elevated levels of elongase-5 also reduced triglycerides in the liver, another desirable goal. Elevated triglycerides are associated with "fatty liver," also known as non-alcoholic fatty liver disease. This can progress to more severe liver diseases such as fibrosis, cirrhosis and cancer.
Further research is needed to define the exact biological mechanisms at work in this process, and determine what the fatty acids do that affects carbohydrate and triglyceride metabolism, he said. It appears that high fat diets suppress elongase-5 activity...
Subscribe to:
Posts (Atom)