A natural cannabis-like chemical in the brain may hold the key to keeping couch potatoes slim, early research suggests.
Scientists in the US found that blocking the compound allowed mice to gorge on high fat food and take little exercise without putting on weight or becoming unhealthy.
The genetically modified animals produced limited amounts of the endocannabinoid 2-AG, a chemical related to the active ingredient in cannabis.
All mammalian brains, including those of humans, contain 2-AG, which is believed to control neural circuits involved in metabolism.
"We discovered that these mice were resistant to obesity because they burned fat calories much more efficiently than normal mice do," said study leader Professor Daniele Piomelli, from the University of California at Irvine.
"We had known that endocannabinoids play a critical role in cell energy regulation, but this is the first time we found a target where this occurs."
The mice stayed slim because they developed a hyperactive form of "brown fat" - a special type of fat that generates heat and keeps animals warm.
Not only did they not gain weight when fed a high-fat diet, but they failed to develop any of the expected signs of metabolic syndrome. This is a combination of problems such as obesity and high blood pressure which increase the risk of heart disease and diabetes...
Wednesday, March 14, 2012
The genetic tweak that 'could help us stay cancer free and remain thin no matter how much we eat'
Scientists have made a potential breakthrough against both cancer and obesity after identifying a way of modifying a gene that controls cell growth.
Mice given an extra copy of the anti-cancer gene Pten were less prone to weight gain and were more resistant to the disease.
The Pten gene is key in controlling cell growth in both mice and humans.
The study by the Spanish National Cancer Research Center also found that the creatures with adapted genes lived longer...
Mice given an extra copy of the anti-cancer gene Pten were less prone to weight gain and were more resistant to the disease.
The Pten gene is key in controlling cell growth in both mice and humans.
The study by the Spanish National Cancer Research Center also found that the creatures with adapted genes lived longer...
Fighting obesity without exercise or healthy diet possible? (Research)
Tired of trying everything but still not losing that weight? Here’s new research which might help you.
Blocking a brain compound may have a magical effect in burning fat, even if you gorge yourself and avoid the gym, a study reveals. For instance, mice modified to limit production of the brain compound, an endocannabinoid called 2-AG, did not gain any weight, even after being fed high fat diets and becoming sluggish. Neither did they develop any signs of obesity and high blood pressure linked ith cardiovascular disease and diabetes, the journal Cell Metabolism reported...
Blocking a brain compound may have a magical effect in burning fat, even if you gorge yourself and avoid the gym, a study reveals. For instance, mice modified to limit production of the brain compound, an endocannabinoid called 2-AG, did not gain any weight, even after being fed high fat diets and becoming sluggish. Neither did they develop any signs of obesity and high blood pressure linked ith cardiovascular disease and diabetes, the journal Cell Metabolism reported...
Genetic Tweak Helps Mice Avoid Cancer, Obesity: Study
New research offers potential insight into the connection between cancer, obesity and longevity in humans by showing that genetically modified mice live longer, skinnier and almost cancer-free lives.
There are quite a few differences between mice and humans, especially in regard to the type of fat that's apparently affected by the genetic tweak, so there's no way to know if the research could lead to benefits in humans. Even if medications based on the research are developed, no one knows what the side effects in people might be or their eventual cost...
There are quite a few differences between mice and humans, especially in regard to the type of fat that's apparently affected by the genetic tweak, so there's no way to know if the research could lead to benefits in humans. Even if medications based on the research are developed, no one knows what the side effects in people might be or their eventual cost...
Sunday, March 04, 2012
Heart Hormone Linked to Calorie-Burning Brown Fat
You may have heard about brown fat -- a unique type of fat that acts like a furnace in the body to burn calories instead of storing them as excess weight.
Adults don’t have much brown fat, but a new study suggests that hormones produced by the heart just might help them make more.
Researchers found that the hormones, known as cardiac natriuretic peptides, caused regular energy-storing white fat cells to turn into energy-burning brown fat in mice.
If studies show the same thing in humans, the heart hormone may hold the key to an effective weight loss treatment, says researcher Sheila Collins, PhD, of Sanford-Burnham Medical Research Institute in Orlando, Fla.
The study appears online in the Journal of Clinical Investigation.
“These hormones are involved in fluid regulation, but we showed in this study that they also play a role in breaking down fat,” she says.
Brown Fat and Heart Hormones
Collins and colleagues have long studied how the body’s adrenaline system regulates fat storage and weight loss.
In their latest work, they showed that the heart-derived hormones activate the same fat-burning process as the adrenaline pathway and that the two systems can work together to promote the browning of fat cells.
When they exposed mice to cold, the mice exhibited elevated amounts of natriuretic peptides in their circulatory systems, which turned on the fat-burning brown fat...
Adults don’t have much brown fat, but a new study suggests that hormones produced by the heart just might help them make more.
Researchers found that the hormones, known as cardiac natriuretic peptides, caused regular energy-storing white fat cells to turn into energy-burning brown fat in mice.
If studies show the same thing in humans, the heart hormone may hold the key to an effective weight loss treatment, says researcher Sheila Collins, PhD, of Sanford-Burnham Medical Research Institute in Orlando, Fla.
The study appears online in the Journal of Clinical Investigation.
“These hormones are involved in fluid regulation, but we showed in this study that they also play a role in breaking down fat,” she says.
Brown Fat and Heart Hormones
Collins and colleagues have long studied how the body’s adrenaline system regulates fat storage and weight loss.
In their latest work, they showed that the heart-derived hormones activate the same fat-burning process as the adrenaline pathway and that the two systems can work together to promote the browning of fat cells.
When they exposed mice to cold, the mice exhibited elevated amounts of natriuretic peptides in their circulatory systems, which turned on the fat-burning brown fat...
‘Epigenetics’ May Help Obese Persons; Other Uses Include Treatment of Aging, Inherited Diseases and Cancer
A new study at Sydney's Victor Chang Cardiac Research Institute showed that traits can be changed through "epigenetic" changes, which could have implications for a number of trends and changes in our population, such as the obesity epidemic.
Epigenetics is the study of heritable changes in gene expression or cellular phenotype caused by mechanisms other than changes in the underlying DNA sequence. It considers how genes are switched on or off, usually through an environmental stimulus, such as a change in diet.
However, unlike the genetic changes, epigenetic changes do not involve permanent mutations in the genetic code.
In their study, the researchers fed a group of mice a diet rich in supplements such as folate, zinc and vitamin B12, which help to suppress obesity in mice by turning a particular gene off.
The researchers found that when the diet was continued in the lean mice over five generations, the epigenetic effects were inherited which resulted in the increase in the proportion of lean and healthy specimens in each subsequent generation, without any change to the genetic code of the mice...
Epigenetics is the study of heritable changes in gene expression or cellular phenotype caused by mechanisms other than changes in the underlying DNA sequence. It considers how genes are switched on or off, usually through an environmental stimulus, such as a change in diet.
However, unlike the genetic changes, epigenetic changes do not involve permanent mutations in the genetic code.
In their study, the researchers fed a group of mice a diet rich in supplements such as folate, zinc and vitamin B12, which help to suppress obesity in mice by turning a particular gene off.
The researchers found that when the diet was continued in the lean mice over five generations, the epigenetic effects were inherited which resulted in the increase in the proportion of lean and healthy specimens in each subsequent generation, without any change to the genetic code of the mice...
The role of the brain in obesity
Researchers from the French Inserm institute have tested young mice with a diet rich in sugar and fat… And guess what? This diet completely modified their enteric nervous system (ENS).
In addition to our “principal” brain, protected by the skull, our organism is helped by a “second” brain: a group of nearly 100 million neurons lodged in the digestive tube – the enteric nervous system (ENS). And its main job? To regulate digestive function, such as gastric drainage, colonic transit, absorption of nutrients and the regulation of food intake...
In addition to our “principal” brain, protected by the skull, our organism is helped by a “second” brain: a group of nearly 100 million neurons lodged in the digestive tube – the enteric nervous system (ENS). And its main job? To regulate digestive function, such as gastric drainage, colonic transit, absorption of nutrients and the regulation of food intake...
Obesity could be INFECTIOUS: Gut microbe imbalance is catching, study finds
We all know of couples who piled on the pounds once they married and fat friends who seem to encourage each others bad eating habits.
But scientists have now claimed that chubbiness could be catching.
A study from Yale University found that both obesity and liver disease can be triggered by a family of proteins called inflammasomes that alter the balance of microbes in the stomach.
Amazingly, this altered intestinal environment can be passed on - making obesity an infectious condition.
The finding came to light during a study on stomach bacteria in mice...
But scientists have now claimed that chubbiness could be catching.
A study from Yale University found that both obesity and liver disease can be triggered by a family of proteins called inflammasomes that alter the balance of microbes in the stomach.
Amazingly, this altered intestinal environment can be passed on - making obesity an infectious condition.
The finding came to light during a study on stomach bacteria in mice...
Mutation of fat-related gene raises risk of obesity: study
A team of researchers from Kyoto University and a French national laboratory have become the world's first to discover that a mutation in a gene related to the detection of fats that enter the body raises the risk of obesity when fatty meals are eaten, according to the online version of the journal Nature posted Monday.
The gene, called GPR120, can also cause fatty liver if it mutates, because in such a case, the organ's ability to burn fat diminishes.
"Diagnosing the gene could help prevent symptoms resulting from metabolic syndrome and their treatment," said Gozo Tsujimoto, a Kyoto University professor and member of the team.
The international team gave fatty feed to two groups of mice -- one in which the GPR120 gene was deactivated and the other in which it was left active. The team found the mice in the group with the deactivated gene gained 15 percent more weight than the other group, while the total amount of body fat turned out to be double the amount in the mice with the normal gene.
The research also showed that the mice with deactivated GPR120 gene exhibited symptoms of fatty liver and diabetes...
The gene, called GPR120, can also cause fatty liver if it mutates, because in such a case, the organ's ability to burn fat diminishes.
"Diagnosing the gene could help prevent symptoms resulting from metabolic syndrome and their treatment," said Gozo Tsujimoto, a Kyoto University professor and member of the team.
The international team gave fatty feed to two groups of mice -- one in which the GPR120 gene was deactivated and the other in which it was left active. The team found the mice in the group with the deactivated gene gained 15 percent more weight than the other group, while the total amount of body fat turned out to be double the amount in the mice with the normal gene.
The research also showed that the mice with deactivated GPR120 gene exhibited symptoms of fatty liver and diabetes...
Animal study finds surprising clues to obesity-induced infertility
Infertility is common among obese women, but the reasons remain poorly understood and few treatments exist. Now a team of Johns Hopkins Children’s Center scientists, conducting experiments in mice, has uncovered what it considers surprising evidence that insulin resistance, long considered a prime suspect, has little to do with infertility in women with type 2 diabetes, polycystic ovary syndrome or metabolic syndrome, all obesity-related conditions in which the body becomes desensitized to insulin and loses the ability to regulate blood sugar.
In a report published online Nov.10 in the journal Diabetes, the Johns Hopkins scientists say that the real culprit appears to be insulin sensitivity in the ovaries and the pituitary.
The Johns Hopkins team said that its findings show that these organs escape insulin resistance and, awash with high levels of circulating insulin common in obesity, develop abnormal cell signaling that disrupts ovulation and eventually leads to infertility.
“Our findings suggest that the focus should shift from treating insulin resistance in peripheral tissue to taming insulin sensitivity in the pituitary and ovaries,” said lead investigator Sheng Wu, of the Johns Hopkins Children’s Center. Scientists traditionally have treated obesity-induced infertility by lowering blood insulin to counter the effects of insulin resistance...
In a report published online Nov.10 in the journal Diabetes, the Johns Hopkins scientists say that the real culprit appears to be insulin sensitivity in the ovaries and the pituitary.
The Johns Hopkins team said that its findings show that these organs escape insulin resistance and, awash with high levels of circulating insulin common in obesity, develop abnormal cell signaling that disrupts ovulation and eventually leads to infertility.
“Our findings suggest that the focus should shift from treating insulin resistance in peripheral tissue to taming insulin sensitivity in the pituitary and ovaries,” said lead investigator Sheng Wu, of the Johns Hopkins Children’s Center. Scientists traditionally have treated obesity-induced infertility by lowering blood insulin to counter the effects of insulin resistance...
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