Sunday, January 30, 2011
New molecular player responsible for regulation of appetite and metabolism
A study by researchers at Mayo Clinic's campus in Florida and Washington University School of Medicine adds 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, neuroscientists identified a new molecular player responsible for the regulation of appetite and metabolism...
Study suggests designer probiotics could help cut obesity
Targeted probiotics could affect the physiology of human fat cells and potentially prevent or help treat conditions such as obesity, according to new Irish research.
Recently published in Microbiology, the study from scientists at Teagasc (the Irish Agriculture and Food Development Authority), University College Cork and the Alimentary Pharmabiotic Centre examined whether a lactobacillus strain with CLA (conjugated linoleic acid) influenced fat tissue composition in mice.
Previous research from Racine et al. (2010) and Thom et al. (2001) has linked fatty acid t10, c12 CLA consumption with decreased body fat in humans, while other studies suggest that this type of fatty acid inhibits colon cancer cell growth.
Probiotics assists CLA metabolism
In this study, scientists transferred an enzyme-encoding gene from skin bacterium P.acnes to Lactobacillus paracasei and induced it to produce CLA t10, c12, which fed to mice resulted in a fourfold increase of CLA in mouse fat tissue composition (against a second probiotic control strain) showing that live bacteria intake affects metabolism at remote body sites...
Warmer Houses May Increase Obesity
...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...
"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...
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...
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