Cholesterol levels are controlled by a “hormone in the brain” the Daily Mail has reported.
It says the finding offers hope of new treatments to reduce levels of “the dangerous fat”.
The Mail’s story is based on animal research that appears to indicate that blood cholesterol levels are regulated remotely by the central nervous system. The researchers found that increasing levels of a hormone called ghrelin, which is thought to regulate energy intake, caused mice to develop higher levels of cholesterol. The finding that cholesterol can be regulated by the brain could be the basis for new drug treatments, they suggest.
The findings are interesting, but it is important to stress that there are large differences in the way cholesterol affects mice and humans. This is early research that points the way to further research into ghrelin, although more human studies are needed to draw firm conclusions about the brain regulating human blood cholesterol levels. It’s also important to note that, in humans, cholesterol levels can be controlled by diet, exercise and, where necessary, drug treatment...
Saturday, June 19, 2010
Hormone influences sensitivity to sweetness
Scientists have discovered that a blood sugar-regulating hormone may also alter a person's sensitivity to sweet-tasting foods.
Scientists from University of Maryland School of Medicine found that changing the actions of the hormone glucagon could control how foods taste.
"An interesting possibility resulting from our research is that the development of new food additives could change the way you perceive your food, making it taste more or less sweet," said senior author Steven D. Munger, Ph.D., associate professor of anatomy and neurobiology at the University of Maryland School of Medicine.
"From a food industry perspective, such additives could be used to enhance flavour. From a therapeutic perspective, they could be used to treat patients who under-eat or overeat."
When experimented on mice, the researchers found that blocking glucagon's actions using a specific drug made mice less responsive to a sweet solution they were offered. Thus, the actions of these hormones can be directly manipulated in the mouth.
"That leaves open the possibility that we could also enhance sensitivity to sugars by manipulating glucagon in the other direction. That could open doors for food additives to make what we eat taste sweeter without adding more sugar," says Munger.
"Dr. Munger's findings could have great significance for patients who suffer from diabetes, metabolic disorders or obesity," says E. Albert Reece, M.D., Ph.D., M.B.A., acting president of the University of Maryland, Baltimore and John Z. and Akiko K. Bowers Distinguished Professor and dean, University of Maryland School of Medicine...
Scientists from University of Maryland School of Medicine found that changing the actions of the hormone glucagon could control how foods taste.
"An interesting possibility resulting from our research is that the development of new food additives could change the way you perceive your food, making it taste more or less sweet," said senior author Steven D. Munger, Ph.D., associate professor of anatomy and neurobiology at the University of Maryland School of Medicine.
"From a food industry perspective, such additives could be used to enhance flavour. From a therapeutic perspective, they could be used to treat patients who under-eat or overeat."
When experimented on mice, the researchers found that blocking glucagon's actions using a specific drug made mice less responsive to a sweet solution they were offered. Thus, the actions of these hormones can be directly manipulated in the mouth.
"That leaves open the possibility that we could also enhance sensitivity to sugars by manipulating glucagon in the other direction. That could open doors for food additives to make what we eat taste sweeter without adding more sugar," says Munger.
"Dr. Munger's findings could have great significance for patients who suffer from diabetes, metabolic disorders or obesity," says E. Albert Reece, M.D., Ph.D., M.B.A., acting president of the University of Maryland, Baltimore and John Z. and Akiko K. Bowers Distinguished Professor and dean, University of Maryland School of Medicine...
Black Tea Curbs Weight Gain
GUNMA, Japan—Black tea extract suppressed weight gain and fat levels in a recent mice study (doi:10.1016/j.nut.2010.01.019). The Japanese researchers found that black tea extract prevented diet-induced obesity by inhibiting intestinal lipid absorption. They also suggested that the major active component in the black tea extract was the polyphenols.
Using black tea extract, researchers from the Kirin Beverage Company Ltd., Gunma, Japan, prepared a polymerized polyphenol fraction (BTP), and fed it to Male Wistar rats at a concentration of 500 or 1,000 mg/kg body weight. Researchers then measured their plasma lipid levels. Additionally, female mice were fed either a standard or high-fat diet supplemented with 1-percent or 5-percent black tea extract for eight weeks, and changes in body weight were examined.
Both the BTP and black tea extract inhibited pancreatic lipase activity. The black tea extract suppressed increases in rat plasma triglyceride levels in a dose-dependent manner. Furthermore, administration of the 5 percent black tea extract suppressed increases in body weight (P<0.05), parametrial adipose tissue mass and liver lipid content (reduced to 56.9 percent and 81.7 percent of control mice, respectively, P<0.05) in mice fed a high-fat diet.
Using black tea extract, researchers from the Kirin Beverage Company Ltd., Gunma, Japan, prepared a polymerized polyphenol fraction (BTP), and fed it to Male Wistar rats at a concentration of 500 or 1,000 mg/kg body weight. Researchers then measured their plasma lipid levels. Additionally, female mice were fed either a standard or high-fat diet supplemented with 1-percent or 5-percent black tea extract for eight weeks, and changes in body weight were examined.
Both the BTP and black tea extract inhibited pancreatic lipase activity. The black tea extract suppressed increases in rat plasma triglyceride levels in a dose-dependent manner. Furthermore, administration of the 5 percent black tea extract suppressed increases in body weight (P<0.05), parametrial adipose tissue mass and liver lipid content (reduced to 56.9 percent and 81.7 percent of control mice, respectively, P<0.05) in mice fed a high-fat diet.
Fat chance
Throughout the leaner epochs of human history, when food supplies were unreliable, the species would not have survived without a way to hoard calories for later use. That is, without fat. Once a meal has supplied the body’s immediate energy needs, any unused fuel gets converted into long molecules called triglycerides, which are dispatched to fatty tissue where they wait for a signal that the body needs them.
But in an era of high-calorie smorgasbords and 24/7 convenience, unused energy can just pile on year after year, a major reason why one-third of the U.S. adult population is struggling with obesity. Laws of physics — the ones about conservation of matter and energy — dictate that schemes for burning off all that fat are pretty much limited to two options: Diet to lower the amount of energy consumed, or exercise to increase the amount of energy the body needs...
Other than joining a polar bear club, there’s no obvious way to boost your brown fat activity. In May, in the journal Science, Herzig and his colleagues reported that the enzyme COX-2, which is involved in many body processes, plays a role in turning white fat brown. He and his colleagues described experiments in which they rebooted white fat in mice, turning it brown, after increasing the animals’ exposure to COX-2 and mimicking the physiological changes caused by cold. Even more important, mice with new deposits of brown fat lost weight...
But in an era of high-calorie smorgasbords and 24/7 convenience, unused energy can just pile on year after year, a major reason why one-third of the U.S. adult population is struggling with obesity. Laws of physics — the ones about conservation of matter and energy — dictate that schemes for burning off all that fat are pretty much limited to two options: Diet to lower the amount of energy consumed, or exercise to increase the amount of energy the body needs...
Other than joining a polar bear club, there’s no obvious way to boost your brown fat activity. In May, in the journal Science, Herzig and his colleagues reported that the enzyme COX-2, which is involved in many body processes, plays a role in turning white fat brown. He and his colleagues described experiments in which they rebooted white fat in mice, turning it brown, after increasing the animals’ exposure to COX-2 and mimicking the physiological changes caused by cold. Even more important, mice with new deposits of brown fat lost weight...
Scientists identify link between obesity, salt-sensitivity, BP
Medical College of Georgia researchers documented a chain of events in which excess inflammatory factors resulting from excess fat cause the body to retain more sodium and, consequently, more fluid and higher blood pressure.
Dr. Yanbin Dong, geneticist and cardiologist at MCG's Georgia Prevention Institute found that a biomarker in the urine could help identify the most effective therapy for these patients. Dong's team outlined the process that appears to start with fat producing more inflammatory factors, such as interleukin-6, or IL-6.
IL-6 in mice increased production of prostasin, and when it cut fellow protein ENaC it increased its activity and so salt reabsorption. ENaC determines how much sodium to excrete.
Dong said, "It's very special; there are not too many proteases like that. We found that in cells fed IL-6, ENaC gets activated and the cells take in more sodium. It is the last step of your salt reabsorption."...
Dr. Yanbin Dong, geneticist and cardiologist at MCG's Georgia Prevention Institute found that a biomarker in the urine could help identify the most effective therapy for these patients. Dong's team outlined the process that appears to start with fat producing more inflammatory factors, such as interleukin-6, or IL-6.
IL-6 in mice increased production of prostasin, and when it cut fellow protein ENaC it increased its activity and so salt reabsorption. ENaC determines how much sodium to excrete.
Dong said, "It's very special; there are not too many proteases like that. We found that in cells fed IL-6, ENaC gets activated and the cells take in more sodium. It is the last step of your salt reabsorption."...
Protein involved in metabolic dysfunction in obesity identified
A study by Boston University School of Medicine (BUSM) has shown that secreted frizzled-related protein 5 (Sfrp5) is an anti-inflammatory adipokine whose expression is disrupted in animal models of obesity and type 2 diabetes . The research, published in Science, could be key to the development of new approaches to obesity and other metabolic diseases.
Obesity can contribute to metabolic disorders such as type 2 diabetes, which is often associated with a low-grade inflammatory state in adipose tissue . Since adipokine dysregulation is associated with the pathogenesis of obesity-linked disorders, the research team attempted to identify new adipokines by comparing the genetic profile of adipose tissue taken from both lean mice obese mice on a high calorie diet .
Kenneth Walsh, lead author of the study, commented that "Our study shows that Sfrp5 is secreted by adipocytes and that it controls the microenvironment of white adipose tissue under conditions of obesity-induced metabolic stress ...
Obesity can contribute to metabolic disorders such as type 2 diabetes, which is often associated with a low-grade inflammatory state in adipose tissue . Since adipokine dysregulation is associated with the pathogenesis of obesity-linked disorders, the research team attempted to identify new adipokines by comparing the genetic profile of adipose tissue taken from both lean mice obese mice on a high calorie diet .
Kenneth Walsh, lead author of the study, commented that "Our study shows that Sfrp5 is secreted by adipocytes and that it controls the microenvironment of white adipose tissue under conditions of obesity-induced metabolic stress ...
Sunday, June 13, 2010
Mice explain why people are overweight
TOPIC: GENES OF OBESITY: MEDICINE’S NEXT BIG THING?
REPORT: MB #3149
BACKGROUND: Some doctors call obesity the most prevalent, fatal, chronic, and relapsing disorder of the 21st century. It is a leading cause of mortality, morbidity, disability, health care utilization and costs in the U.S. Experts predict the increase in obesity will strain our health care system with millions of additional cases of diabetes, heart disease and disability. Obesity is a disease that impacts more than one-third of the adult American population, which is about 72 million people. More than 66 percent of adult Americans are categorized as being overweight or obese. Since 1960, Americans have increased average heights by 1 inch and average weight by 25 pounds. In 1963, a 10-year-old boy weighed about 74 pounds. Now, the average boy weighs 85 pounds, according to The Obesity Society. Each year, obesity causes about 112,000 excess deaths in America. Obesity is linked to many adverse health effects including high cholesterol, diabetes, hypertension, gallstones, fatty liver disease, sleep apnea, heart failure, birth defects, miscarriages and asthma. Health care costs of American adults with obesity amount to about $147 billion.
GENETIC LINK: The best success stories providing evidence for obesity genes come from several cases of extreme obesity due to mutations of single genes, according to the Centers for Disease Control. Melanocortin 4-receptor gene, which is related to the control of feeding behavior, has been found to be strongly associated with a minority of obesity cases in several populations. Progress in identifying the multiple genes associated with the most common form of obesity has been slow but is accelerating. Single mutations in 11 genes were strongly implicated in 176 cases of obesity worldwide, according to the CDC. Additionally, 50 chromosomal locations relevant to obesity have been mapped with potential causal genes identified in most of those regions...
REPORT: MB #3149
BACKGROUND: Some doctors call obesity the most prevalent, fatal, chronic, and relapsing disorder of the 21st century. It is a leading cause of mortality, morbidity, disability, health care utilization and costs in the U.S. Experts predict the increase in obesity will strain our health care system with millions of additional cases of diabetes, heart disease and disability. Obesity is a disease that impacts more than one-third of the adult American population, which is about 72 million people. More than 66 percent of adult Americans are categorized as being overweight or obese. Since 1960, Americans have increased average heights by 1 inch and average weight by 25 pounds. In 1963, a 10-year-old boy weighed about 74 pounds. Now, the average boy weighs 85 pounds, according to The Obesity Society. Each year, obesity causes about 112,000 excess deaths in America. Obesity is linked to many adverse health effects including high cholesterol, diabetes, hypertension, gallstones, fatty liver disease, sleep apnea, heart failure, birth defects, miscarriages and asthma. Health care costs of American adults with obesity amount to about $147 billion.
GENETIC LINK: The best success stories providing evidence for obesity genes come from several cases of extreme obesity due to mutations of single genes, according to the Centers for Disease Control. Melanocortin 4-receptor gene, which is related to the control of feeding behavior, has been found to be strongly associated with a minority of obesity cases in several populations. Progress in identifying the multiple genes associated with the most common form of obesity has been slow but is accelerating. Single mutations in 11 genes were strongly implicated in 176 cases of obesity worldwide, according to the CDC. Additionally, 50 chromosomal locations relevant to obesity have been mapped with potential causal genes identified in most of those regions...
Research team finds fat-melting protein, development of weight-loss drug likely
A research team has found a microphage-derived protein is capable of breaking down fat masses, which it hopes will lead to the development of a weight-loss drug.
The research team, led by University of Tokyo professor Toru Miyazaki, discovered the macrophage-derived protein, AIM, in 1999. In a bid to examine how the protein functions, they engineered a mouse not to produce AIM and found it grew fatter than ordinary mice eating the same amounts of food.
Researchers then injected AIM into fat cells in the engineered mouse, and confirmed that its fat masses were reduced in size by three-fourths in 72 hours...
The research team, led by University of Tokyo professor Toru Miyazaki, discovered the macrophage-derived protein, AIM, in 1999. In a bid to examine how the protein functions, they engineered a mouse not to produce AIM and found it grew fatter than ordinary mice eating the same amounts of food.
Researchers then injected AIM into fat cells in the engineered mouse, and confirmed that its fat masses were reduced in size by three-fourths in 72 hours...
Tuesday, June 08, 2010
The brain may control cholesterol
Cholesterol levels are controlled by a “hormone in the brain” the Daily Mail has reported. It says the finding offers hope of new treatments to reduce levels of “the dangerous fat”.
The Mail’s story is based on animal research that appears to indicate that blood cholesterol levels are regulated remotely by the central nervous system. The researchers found that increasing levels of a hormone called ghrelin, which is thought to regulate energy intake, caused mice to develop higher levels of cholesterol. The finding that cholesterol can be regulated by the brain could be the basis for new drug treatments, they suggest.
The findings are interesting, but it is important to stress that there are large differences in the way cholesterol affects mice and humans. This is early research that points the way to further research into ghrelin, although more human studies are needed to draw firm conclusions about the brain regulating human blood cholesterol levels. It’s also important to note that, in humans, cholesterol levels can be controlled by diet, exercise and, where necessary, drug treatment..
The researchers found that giving the mice the hormone ghrelin for one week not only caused the expected increase in body fat, but also significantly increased total blood cholesterol levels, compared with a control group. Levels of blood glucose and fats called triglycerides remained unchanged.
They also found that when they genetically deleted or blocked the melanocortin receptor (MC4R) in the central nervous system of the mice, it produced increased levels of 'good' HDL cholesterol. They thought part of the reason for this might be that the neural circuit reduces the uptake of cholesterol by the liver...
The Mail’s story is based on animal research that appears to indicate that blood cholesterol levels are regulated remotely by the central nervous system. The researchers found that increasing levels of a hormone called ghrelin, which is thought to regulate energy intake, caused mice to develop higher levels of cholesterol. The finding that cholesterol can be regulated by the brain could be the basis for new drug treatments, they suggest.
The findings are interesting, but it is important to stress that there are large differences in the way cholesterol affects mice and humans. This is early research that points the way to further research into ghrelin, although more human studies are needed to draw firm conclusions about the brain regulating human blood cholesterol levels. It’s also important to note that, in humans, cholesterol levels can be controlled by diet, exercise and, where necessary, drug treatment..
The researchers found that giving the mice the hormone ghrelin for one week not only caused the expected increase in body fat, but also significantly increased total blood cholesterol levels, compared with a control group. Levels of blood glucose and fats called triglycerides remained unchanged.
They also found that when they genetically deleted or blocked the melanocortin receptor (MC4R) in the central nervous system of the mice, it produced increased levels of 'good' HDL cholesterol. They thought part of the reason for this might be that the neural circuit reduces the uptake of cholesterol by the liver...
Genes and obesity
Thick or thin. Whichever you are, it may not be your fault.
HealthFirst reporter Leslie Toldo says our weight may boil down to a genetic link we share with mice.
Over half of us humans are overweight. That's not really new, but for some, that extra fat may have more to do with destiny than lifestyle.
Lisa Bohner has one wish. "To have life again. To be normal."
She and her 455 pounds struggle every step, every day. "Right now ... I only merely exist."
But this nearly quarter-ton woman may share a genetic link with a one-ounce mouse.
"It's a way that we can illustrate using mouse models with specific genetic characteristics to dissect these processes that are so common in the human population," Dr. Philip Wood, DVM, PhD, said.
Wood created six mouse models in his lab, then inactivated fat-burning genes in each one. Some got fat. Others built up insulin resistance. Others stayed healthy.
Now, he's matching each mouse with a two-footed counterpart -- a person with the same genetic makeup. "We can sort of find the tipping point, if you will. When does obesity show up? When does diabetes show up? When does high blood pressure show up?"
The goal is to indentify people whose genes predispose them to being fat and all the diseases that follow, and find therapies to turn off those switches...
HealthFirst reporter Leslie Toldo says our weight may boil down to a genetic link we share with mice.
Over half of us humans are overweight. That's not really new, but for some, that extra fat may have more to do with destiny than lifestyle.
Lisa Bohner has one wish. "To have life again. To be normal."
She and her 455 pounds struggle every step, every day. "Right now ... I only merely exist."
But this nearly quarter-ton woman may share a genetic link with a one-ounce mouse.
"It's a way that we can illustrate using mouse models with specific genetic characteristics to dissect these processes that are so common in the human population," Dr. Philip Wood, DVM, PhD, said.
Wood created six mouse models in his lab, then inactivated fat-burning genes in each one. Some got fat. Others built up insulin resistance. Others stayed healthy.
Now, he's matching each mouse with a two-footed counterpart -- a person with the same genetic makeup. "We can sort of find the tipping point, if you will. When does obesity show up? When does diabetes show up? When does high blood pressure show up?"
The goal is to indentify people whose genes predispose them to being fat and all the diseases that follow, and find therapies to turn off those switches...
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