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...
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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...
Sunday, January 09, 2011
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...
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