A Recent medical research has looked at the effect of the Maitake mushroom (Grifola frondosa) on a variety of common cancers. These mushrooms are native to the northeastern part of Japan and North America. They have been used as medicinal mushrooms for centuries in traditional Chinese and Japanese herbal medicine. They are also commonly used in Chinese and Japanese cooking. Numerous benefits of the Maitake have been proposed, ranging from anti-cancer effects to treatment for blood pressure, diabetes, high cholesterol, obesity and hepatitis B infection. Most research has been focused on the use of maitake D-fraction, which is extracted from the Maitake mushroom...
Trials involving maitake mushrooms for other cancers have taken place. In a 1995 report from New York, researchers concluded that maitake D-fraction was able to activate the immune systems of mice that had been injected with liver cancer cells. A further study published in 1997 in the Annals of the New York Academy of Science found that maitake D-fraction was able to enhance the immune system and inhibit the spread of tumours in mice implanted with breast cancer."
Monday, December 28, 2009
Secrets to longer, cancer-free life
"Previous research on mice and rats has shown that both calorie restriction and endurance exercise protect them against many chronic diseases including obesity, diabetes, cardiovascular disease and some types of cancer. However, the research has shown that only CR increases the animals' maximum life span by up to 50 percent. These animal studies suggest that leanness is a key factor in the prevention of age-associated disease, but reducing caloric intake is needed to slow down ageing...
Previous evidence from different organisms (fruit flies and mice) have shown that dietary restriction increases longevity, but with a potential negative side effect of diminished fertility. So the female fruit fly reproduces less frequently with a reduced litter size on a low calorie diet, but its reproductive span lasts longer. This is the result of an evolutionary trait, as scientists believe: essential nutrients are diverted towards survival instead of reproduction."
Previous evidence from different organisms (fruit flies and mice) have shown that dietary restriction increases longevity, but with a potential negative side effect of diminished fertility. So the female fruit fly reproduces less frequently with a reduced litter size on a low calorie diet, but its reproductive span lasts longer. This is the result of an evolutionary trait, as scientists believe: essential nutrients are diverted towards survival instead of reproduction."
Sleep Apnea Takes Another Victim: The Liver
The Link Between Sleep Apnea And Liver Disease
The Bern research involved studies of normal mice kept in a low oxygen environment for seven days; the control group was kept in a normal oxygen environment. After seven days, the mice in the low oxygen atmosphere showed pronounced fat deposits and inflammation in the livers. These effects were not observed in the normal oxygen group.
Also observed were the genes of the low oxygen group. The genes responsible for fat synthesis were shown to be highly active, while the genes responsible for fat breakdown showed reduced activity.
The third observation of the low oxygen group was that the mice were less sensitive to insulin than the control group."
The Bern research involved studies of normal mice kept in a low oxygen environment for seven days; the control group was kept in a normal oxygen environment. After seven days, the mice in the low oxygen atmosphere showed pronounced fat deposits and inflammation in the livers. These effects were not observed in the normal oxygen group.
Also observed were the genes of the low oxygen group. The genes responsible for fat synthesis were shown to be highly active, while the genes responsible for fat breakdown showed reduced activity.
The third observation of the low oxygen group was that the mice were less sensitive to insulin than the control group."
High-sugar diet alters intestinal bacteria, making losing weight more difficult
"A report published in the new journal Science Translational Medicine has made an interesting discovery concerning the relationship between sugar intake and the balance of intestinal flora. Researchers have discovered that a diet high in sugar and fat substantially alters the bacterial composition in the gut, making it difficult to maintain a healthy weight.
Dr. Jeffrey Gordon of Washington University in St. Louis has been accumulating research for years that highlights the role intestinal bacteria plays in regulating bodily weight. Intestinal flora, sometimes called "good" bacteria, is vital for the proper digestion of food and assimilation of nutrients into the blood. When digestive bacteria is out of balance or otherwise altered, the body is unable to convert otherwise indigestible foods into digestible form.
The research, conducted on mice, experimented with implanting various strains of bacteria into mice in order to observe their effects. The two primary divisions of bacteria, Firmicutes and Bacteroidetes, compose approximately 90 percent of all bacteria. Studies by Dr. Gordon have revealed that Firmicutes bacteria are more efficient at digesting food that the body is unable to digest on its own.
With this in mind, Dr. Gordon decided to experiment with the various bacteria in gnotobiotic mice, or mice which had no bacteria in their intestines because they were raised in a sterile environment. What he found was that gnotobiotic mice who received bacteria from obese mice became obese as well. Similarly, those gnotobiotic mice who received lean-mice bacteria tended more towards leanness.
The same experiment was tried with human intestinal bacteria and similar results were achieved. What also became apparent was that mice who received bacteria from lean human intestines had a much higher proportion of Bacteroidetes than they did Firmicutes.
These mice, who began with a low-fat diet rich in healthy plants, were switched to a high-sugar, high-fat diet following the implant of the lean human bacteria. It was discovered that within 24 hours, the two phyla compositions switched resulting in the Firmicutes bacteria becoming more dominant than the Bacteroidetes bacteria."
Dr. Jeffrey Gordon of Washington University in St. Louis has been accumulating research for years that highlights the role intestinal bacteria plays in regulating bodily weight. Intestinal flora, sometimes called "good" bacteria, is vital for the proper digestion of food and assimilation of nutrients into the blood. When digestive bacteria is out of balance or otherwise altered, the body is unable to convert otherwise indigestible foods into digestible form.
The research, conducted on mice, experimented with implanting various strains of bacteria into mice in order to observe their effects. The two primary divisions of bacteria, Firmicutes and Bacteroidetes, compose approximately 90 percent of all bacteria. Studies by Dr. Gordon have revealed that Firmicutes bacteria are more efficient at digesting food that the body is unable to digest on its own.
With this in mind, Dr. Gordon decided to experiment with the various bacteria in gnotobiotic mice, or mice which had no bacteria in their intestines because they were raised in a sterile environment. What he found was that gnotobiotic mice who received bacteria from obese mice became obese as well. Similarly, those gnotobiotic mice who received lean-mice bacteria tended more towards leanness.
The same experiment was tried with human intestinal bacteria and similar results were achieved. What also became apparent was that mice who received bacteria from lean human intestines had a much higher proportion of Bacteroidetes than they did Firmicutes.
These mice, who began with a low-fat diet rich in healthy plants, were switched to a high-sugar, high-fat diet following the implant of the lean human bacteria. It was discovered that within 24 hours, the two phyla compositions switched resulting in the Firmicutes bacteria becoming more dominant than the Bacteroidetes bacteria."
Friday, December 25, 2009
Brown Fat Revelations May Lead to New Weight Loss Drugs
"Five years ago this February, Aaron Cypess had an epiphany about fat. A fellow in endocrinology at Boston’s Beth Israel Deaconess Medical Center, Cypess happened to be attending a lecture in which a doctor presented images of human PET scans. At one point, Cypess recalls, the doctor indicated an area corresponding to the neck and said, rather dismissively, “Oh, that’s brown fat.” Cypess was taken aback. After the lecture, he approached the doctor and told him he must have been mistaken: Everyone knows there’s no brown fat in human adults. The doctor responded, “Yeah, there is. We see it all the time.” Cypess paused. “Wait a minute,” he said. “Really?”
Brown fat has long been known to exist in infants and animals such as mice, but until recently scientists thought it disappeared before human adulthood, leaving only the white fat that’s associated with weight gain. Unlike white fat, which stores energy, chestnut-colored brown fat burns it. Brown fat cells contain a large supply of organelles called mitochondria, and an enzyme that allows them to release energy from food calories directly as heat. This spring, multiple studies in The New England Journal of Medicine—including one co-authored by Cypess, now a research associate at the Joslin Diabetes Center in Boston—confirmed that not only is brown fat common in adults, it’s also important to metabolism: Younger, thinner people have more detectable brown fat than their older, pudgier counterparts...
Animal studies also suggest brown fat boosts weight loss. Last year, Stockholm University scientists found that mice that could not make brown fat gained weight 50 percent faster than mice that could. In a 2008 study, mice fed a high-fat diet and kept at room temperature ended up nearly four times heavier than mice fed the same diet and housed at 39 F."
Brown fat has long been known to exist in infants and animals such as mice, but until recently scientists thought it disappeared before human adulthood, leaving only the white fat that’s associated with weight gain. Unlike white fat, which stores energy, chestnut-colored brown fat burns it. Brown fat cells contain a large supply of organelles called mitochondria, and an enzyme that allows them to release energy from food calories directly as heat. This spring, multiple studies in The New England Journal of Medicine—including one co-authored by Cypess, now a research associate at the Joslin Diabetes Center in Boston—confirmed that not only is brown fat common in adults, it’s also important to metabolism: Younger, thinner people have more detectable brown fat than their older, pudgier counterparts...
Animal studies also suggest brown fat boosts weight loss. Last year, Stockholm University scientists found that mice that could not make brown fat gained weight 50 percent faster than mice that could. In a 2008 study, mice fed a high-fat diet and kept at room temperature ended up nearly four times heavier than mice fed the same diet and housed at 39 F."
New gene discovery regulates obesity and diabetes
"Researchers at Boston University School of Medicine, US have chanced upon the discovery of a new gene called Brd 2 that makes mice enormously fat but protects them from Type 2 diabetes.
Research showed that while complete absence of the gene was fatal, in case of a single, genetic change in the Brd2 gene of mice, thereby reducing its expression, they became severely obese but did not go on to develop Type 2 diabetes. Usually in both mice and men, chronic obesity commonly leads to Type 2 diabetes, followed by other serious conditions such as heart disease, kidney and nerve damage, osteoporosis, blindness and circulation problems in the feet that may require amputation. This result therefore came as a surprise to doctors, part of this research.
It is being predicted that with rising obesity cases, there will be around 366 million diabetic individuals worldwide by 2030. The research has been undertaken is because of the urgent need to arrive at an understanding of the linkage between obesity and diabetes, so that new drugs and therapies can be developed for treatment."
Research showed that while complete absence of the gene was fatal, in case of a single, genetic change in the Brd2 gene of mice, thereby reducing its expression, they became severely obese but did not go on to develop Type 2 diabetes. Usually in both mice and men, chronic obesity commonly leads to Type 2 diabetes, followed by other serious conditions such as heart disease, kidney and nerve damage, osteoporosis, blindness and circulation problems in the feet that may require amputation. This result therefore came as a surprise to doctors, part of this research.
It is being predicted that with rising obesity cases, there will be around 366 million diabetic individuals worldwide by 2030. The research has been undertaken is because of the urgent need to arrive at an understanding of the linkage between obesity and diabetes, so that new drugs and therapies can be developed for treatment."
Tuesday, December 22, 2009
Inhibiting The Cellular Process Autophagy Makes Mice Leaner
"Recent data have indicated that the more brown fat cells a person has the lower their body mass. This contrasts with what is known for white fat cells, the more white fat cells a person has the greater their body mass. It has been suggested that manipulating the development of fat cells so that they become brown fat cells rather than white fat cells might be an approach to treat obesity.
However, before such an approach can be developed more needs to be learned about the mechanisms regulating the formation, expansion, and interconversion of these two cell types.
New research, performed by Mark Czaja and colleagues, at Albert Einstein College of Medicine, New York, has now identified a cellular process that regulates the formation of the distinct fat cell types in mice. The research appears in the Journal of Clinical Investigation.
Specifically, in mice with fat cells unable to perform the cellular process known as autophagy, there were fewer white fat cells and more brown fat cells than normal. Further, these mice were leaner than normal."
However, before such an approach can be developed more needs to be learned about the mechanisms regulating the formation, expansion, and interconversion of these two cell types.
New research, performed by Mark Czaja and colleagues, at Albert Einstein College of Medicine, New York, has now identified a cellular process that regulates the formation of the distinct fat cell types in mice. The research appears in the Journal of Clinical Investigation.
Specifically, in mice with fat cells unable to perform the cellular process known as autophagy, there were fewer white fat cells and more brown fat cells than normal. Further, these mice were leaner than normal."
Saturday, December 19, 2009
Adiponectin in insulin resistance: lessons from translational research
"Adiponectin is an adipose tissue–secreted endogenous insulin sensitizer, which plays a key role as a mediator of peroxisome proliferator-activated receptor action. Adiponectin alters glucose metabolism and insulin sensitivity, exhibits antiinflammatory and antiatherogenic properties, and has been linked to several malignancies. Circulating concentrations of adiponectin are determined primarily by genetic factors, nutrition, exercise, and abdominal adiposity. Adiponectin concentrations are lower in subjects with obesity, metabolic syndrome, and cardiovascular disease. Adiponectin knockout mice manifest glucose intolerance, insulin resistance, and hyperlipidemia and tend to develop malignancies especially when on high-fat diets. Animal studies have also shown beneficial effects of adiponectin in rodents in vivo. Circulating concentrations of adiponectin are lower in patients with diabetes, cardiovascular disease, and several malignancies. Studies to date provide promising results for the diagnostic and therapeutic role of adiponectin in obesity, insulin resistance, diabetes, cardiovascular disease, and obesity-associated malignancies."
Fibroblast growth factor 21: from pharmacology to physiology
"Fibroblast growth factor 21 (FGF21) is an atypical member of the FGF family that functions as an endocrine hormone. Pharmacologic studies show that FGF21 has broad metabolic actions in obese rodents and primates that include enhancing insulin sensitivity, decreasing triglyceride concentrations, and causing weight loss. In lean rodents, FGF21 expression is strongly induced in liver by prolonged fasting through a mechanism that involves the nuclear receptor peroxisome proliferator-activated receptor . FGF21, in turn, induces the transcriptional coactivator protein peroxisome proliferator-activated receptor coactivator protein 1 and stimulates hepatic gluconeogenesis, fatty acid oxidation, and ketogenesis. FGF21 also blocks somatic growth and sensitizes mice to a hibernation-like state of torpor. Thus, FGF21 plays a key role in eliciting and coordinating the adaptive starvation response. Interestingly, FGF21 expression is induced in white adipose tissue by peroxisome proliferator-activated receptor , which suggests that it also regulates metabolism in the fed state."
Wednesday, December 16, 2009
When you eat can promote weight loss and fight diabetes, researchers find
"Researchers have long noted that shift workers -- folks like nurses, security personnel and others on the night shift -- are extremely prone to developing metabolic syndrome, a pre-diabetic condition marked by insulin resistance, weight gain around the middle and high cholesterol levels. But why? Do they tend to simply eat too many snacks as they try to stay alert at night or is it related to disruption of the circadian clock, the body's internal master clock in the brain that's set by light exposure? Turns out, according to new research by scientists at the Salk Institute, there's probably another crucial factor: not only is what you eat important to health but when you eat appears to be crucial to weight control and healthy metabolism.
In experiments with mice, researchers at the Salk Institute for Biological Studies discovered there's a daily waxing and waning of thousands of genes in the liver, the organ that's the body's metabolic clearinghouse. And this revving up and slowing down is primarily controlled not just by food intake and not by the body's circadian clock, as was previously assumed...
The Salk researchers' findings, which are set for publication in an upcoming issue of the Proceedings of the National Academy of Sciences, could explain why shift workers are at an unusually high risk for metabolic syndrome, diabetes, high cholesterol levels and obesity."
In experiments with mice, researchers at the Salk Institute for Biological Studies discovered there's a daily waxing and waning of thousands of genes in the liver, the organ that's the body's metabolic clearinghouse. And this revving up and slowing down is primarily controlled not just by food intake and not by the body's circadian clock, as was previously assumed...
The Salk researchers' findings, which are set for publication in an upcoming issue of the Proceedings of the National Academy of Sciences, could explain why shift workers are at an unusually high risk for metabolic syndrome, diabetes, high cholesterol levels and obesity."
Discovery of New Gene Called Brd2 That Regulates Obesity and Diabetes
"The chance discovery of a genetic mutation that makes mice enormously fat but protects them from diabetes has given researchers at Boston University School of Medicine, USA, new insights into the cellular mechanisms that link obesity to Type 2 diabetes. Dr Gerald Denis and his colleagues report their findings in the current issue of The Biochemical Journal.
The researchers were studying the gene, called Brd2, which had not previously been linked to body energy balance. While complete absence of the gene was fatal, Dr Denis found that in mice where there had been a single, genetic change in the Brd2 gene, fortuitously reducing its expression, the mice became severely obese -- but did not go on to develop Type 2 diabetes. This result was very surprising because in both 'mice and men', chronic obesity commonly leads to Type 2 diabetes, with its life-threatening consequences, including heart disease, kidney and nerve damage, osteoporosis, blindness and circulation problems in the feet that can require amputation.
If the mice had been human their weight would be equivalent to approximately 270 kilograms (600 pounds); despite this, they exercised at the same levels as normal mice and, in comparison, lived for a surprisingly long time.
Obesity is linked to the development of Type 2 diabetes, and as obesity levels soar -- it is predicted that there will be around 366 million diabetic individuals worldwide by 2030 -- there is an urgent need for a much deeper biological understanding of the forces that link obesity and diabetes, in order to design new drugs and therapies for treatment."
The researchers were studying the gene, called Brd2, which had not previously been linked to body energy balance. While complete absence of the gene was fatal, Dr Denis found that in mice where there had been a single, genetic change in the Brd2 gene, fortuitously reducing its expression, the mice became severely obese -- but did not go on to develop Type 2 diabetes. This result was very surprising because in both 'mice and men', chronic obesity commonly leads to Type 2 diabetes, with its life-threatening consequences, including heart disease, kidney and nerve damage, osteoporosis, blindness and circulation problems in the feet that can require amputation.
If the mice had been human their weight would be equivalent to approximately 270 kilograms (600 pounds); despite this, they exercised at the same levels as normal mice and, in comparison, lived for a surprisingly long time.
Obesity is linked to the development of Type 2 diabetes, and as obesity levels soar -- it is predicted that there will be around 366 million diabetic individuals worldwide by 2030 -- there is an urgent need for a much deeper biological understanding of the forces that link obesity and diabetes, in order to design new drugs and therapies for treatment."
Tuesday, December 15, 2009
Fatty Food Can Weaken the Immune System
"Fresh evidence that fatty food is bad for our health has come to light: mice fed a lard-based diet over a long period got worse at fighting bacteria in the blood, reveals a thesis from the Sahlgrenska Academy.
The mice fed the lard-based diet derived 60 per cent of their total calories from fat. They were compared with mice fed a low-fat diet, where no more than ten per cent of their calories came from fat. As expected, the mice on the high-fat diet got fatter. A more surprising result was that their immune system was less active. The white blood cells got worse at dealing with bacteria in the blood, which could have contributed to many dying of sepsis."
The mice fed the lard-based diet derived 60 per cent of their total calories from fat. They were compared with mice fed a low-fat diet, where no more than ten per cent of their calories came from fat. As expected, the mice on the high-fat diet got fatter. A more surprising result was that their immune system was less active. The white blood cells got worse at dealing with bacteria in the blood, which could have contributed to many dying of sepsis."
Sunday, December 06, 2009
Pleasant Dietary Habits Are Necessary For Health
"Japanese research group led by Professor Yasuhiko Minokoshi and Dr. Tetsuya Shiuchi, scientists at the National Institute for Physiological Sciences, NIPS, Japan, found that meals stimulated with sweet taste and motivated with its anticipation regularly activates 'orexin' in the brain and it stimulates muscle glucose metabolism via the sympathetic nervous system, thereby reducing blood glucose level in mice. They report their finding in Cell Metabolism published on Dec 2, 2009.
The research group focused on the function of 'orexin' neurons in brain. Orexin is a kind of brain hormones related to sleep/wakefulness and food intake. They found that orexin released in the brain from 'orexin' neurons activates glucose metabolism in muscle but not adipose tissue in mice through the preferential activation of the sympathetic nervous system. Furthermore, they found that a pleasant meal with sweet taste stimulation and its anticipation activates orexin neurons and curbs the rise of blood glucose level by activating muscle metabolism via the sympathetic nervous system.
It is known that orexin plays an important role in the regulation of sleep/wakefulness and autonomic nervous system in human as well as experimental animals. Therefore, this finding implies the strong relationship between habits of diet and our health. Pleasant meal with tasty foods (of course, not high calorie) and with family and friends may prevent hyperglycemia by activating orexin neurons."
The research group focused on the function of 'orexin' neurons in brain. Orexin is a kind of brain hormones related to sleep/wakefulness and food intake. They found that orexin released in the brain from 'orexin' neurons activates glucose metabolism in muscle but not adipose tissue in mice through the preferential activation of the sympathetic nervous system. Furthermore, they found that a pleasant meal with sweet taste stimulation and its anticipation activates orexin neurons and curbs the rise of blood glucose level by activating muscle metabolism via the sympathetic nervous system.
It is known that orexin plays an important role in the regulation of sleep/wakefulness and autonomic nervous system in human as well as experimental animals. Therefore, this finding implies the strong relationship between habits of diet and our health. Pleasant meal with tasty foods (of course, not high calorie) and with family and friends may prevent hyperglycemia by activating orexin neurons."
Friday, December 04, 2009
Balancing Protein Intake, Not Cutting Calories, May Be Key to Long Life
"Getting the correct balance of proteins in our diet may be more important for healthy ageing than reducing calories, new research funded by the Wellcome Trust and Research into Ageing suggests.
The research may help explain why 'dietary restriction' (also known as calorie restriction) -- reducing food intake whilst maintaining sufficient quantities of vitamins, minerals and other important nutrients -- appears to have health benefits. In many organisms, such as the fruit fly (drosophila), mice, rats and the Rhesus monkey, these benefits include living longer."
The research may help explain why 'dietary restriction' (also known as calorie restriction) -- reducing food intake whilst maintaining sufficient quantities of vitamins, minerals and other important nutrients -- appears to have health benefits. In many organisms, such as the fruit fly (drosophila), mice, rats and the Rhesus monkey, these benefits include living longer."
Monday, November 30, 2009
Western Diets Turn on Fat Genes: Energy-Dense Foods May Activate Genes That Ultimately Make Us Obese
"Those extra helpings of gravy and dessert at the holiday table are even less of a help to your waistline than previously thought. According to a new research report recently appearing online in The FASEB Journal, a diet that is high in fat and in sugar actually switches on genes that ultimately cause our bodies to store too much fat.
This means these foods hit you with a double-whammy as the already difficult task of converting high-fat and high-sugar foods to energy is made even harder because these foods also turn our bodies into "supersized fat-storing" machines.
In the research report, scientists show that foods high in fat and sugar stimulate a known opioid receptor, called the kappa opioid receptor, which plays a role in fat metabolism. When this receptor is stimulated, it causes our bodies to hold on to far more fat than our bodies would do otherwise.
According to Traci Ann Czyzyk-Morgan, one of the researchers involved in the work, 'the data presented here support the hypothesis that overactivation of kappa opioid receptors contribute to the development of obesity specifically during prolonged consumption of high-fat, calorically dense diets.'
To make this discovery, Czyzyk-Morgan and her colleagues conducted tests in two groups of mice. One group had the kappa opioid receptor genetically deactivated ('knocked out') and the other group was normal. Both groups were given a high fat, high sucrose, energy dense diet for 16 weeks. While the control group of mice gained significant weight and fat mass on this diet, the mice with the deactivated receptor remained lean. In addition to having reduced fat stores, the mice with the deactivated receptor also showed a reduced ability to store incoming nutrients.
Although more work is necessary to examine what the exact effects would be in humans..."
This means these foods hit you with a double-whammy as the already difficult task of converting high-fat and high-sugar foods to energy is made even harder because these foods also turn our bodies into "supersized fat-storing" machines.
In the research report, scientists show that foods high in fat and sugar stimulate a known opioid receptor, called the kappa opioid receptor, which plays a role in fat metabolism. When this receptor is stimulated, it causes our bodies to hold on to far more fat than our bodies would do otherwise.
According to Traci Ann Czyzyk-Morgan, one of the researchers involved in the work, 'the data presented here support the hypothesis that overactivation of kappa opioid receptors contribute to the development of obesity specifically during prolonged consumption of high-fat, calorically dense diets.'
To make this discovery, Czyzyk-Morgan and her colleagues conducted tests in two groups of mice. One group had the kappa opioid receptor genetically deactivated ('knocked out') and the other group was normal. Both groups were given a high fat, high sucrose, energy dense diet for 16 weeks. While the control group of mice gained significant weight and fat mass on this diet, the mice with the deactivated receptor remained lean. In addition to having reduced fat stores, the mice with the deactivated receptor also showed a reduced ability to store incoming nutrients.
Although more work is necessary to examine what the exact effects would be in humans..."
Thursday, November 26, 2009
When You Eat Is As Vital As What You Eat
"An India-American researcher has said that when you eat may be as vital as what you eat.
Experiments in mice showed that the daily waxing and waning of thousands of genes in the liver - the body's metabolic clearing house - is generally controlled by intake of food and not by the body's circadian clock as conservative wisdom believes...
The studies by Salk researchers could clarify why shift workers are oddly prone to diabetes, high cholesterol levels and obesity."
Experiments in mice showed that the daily waxing and waning of thousands of genes in the liver - the body's metabolic clearing house - is generally controlled by intake of food and not by the body's circadian clock as conservative wisdom believes...
The studies by Salk researchers could clarify why shift workers are oddly prone to diabetes, high cholesterol levels and obesity."
Blocked receptor may prevent weight gain
"Drug-based weight loss therapies try to stop the brain from sending hunger signals to the body. These therapies tend to be fairly ineffective. Now researchers have discovered that if certain receptors are blocked in mice, they may be resistant to gaining fat...
They found that if they blocked NPY receptors (Y1) in the peripheral tissues of mice fed with high calorie diets, those mice were resistant to gaining body weight and fat."
They found that if they blocked NPY receptors (Y1) in the peripheral tissues of mice fed with high calorie diets, those mice were resistant to gaining body weight and fat."
Molecule that makes obese people develop diabetes discovered
"European researchers have discovered a molecule that they believe could play a role in causing diabetes in obese people.
They found that obese people have large amounts of the chemokine molecule CXCL5, produced by certain cells in fatty tissue.
They then discovered that an experimental treatment aimed at inhibiting the action of CXCL5 could help to protect obese mice from developing type-2 diabetes."
They found that obese people have large amounts of the chemokine molecule CXCL5, produced by certain cells in fatty tissue.
They then discovered that an experimental treatment aimed at inhibiting the action of CXCL5 could help to protect obese mice from developing type-2 diabetes."
New Study Shows CoQ10 May Prevent Obesity-Related Health Problems
"Obesity is an ever growing problem with numerous health issues associated with it. One of those issues is called fatty liver. Fatty liver, also called steatosis, is the collection of excessive amounts of triglycerides and other fats inside liver cells. When fatty liver is left untreated, it can contribute to many other illnesses. But, a recent animal study indicates that coenzyme Q10 (CoQ10) might hamper the development of fatty liver that is related to obesity.
Animal Study Suggests Positive Affects of CoQ10 on Fatty Liver
Biochemical Pharmacology published findings related to mice that were fed a high fructose high fat diet. The mice that had their diet enhanced with CoQ10 showed decreased levels of inflammatory and metabolic stress markers in their livers when compared to those that were strictly provided the high fructose high fat diet. The supplement did not seem to have any effect on obesity levels or the levels of oxidised fat in other tissues."
Animal Study Suggests Positive Affects of CoQ10 on Fatty Liver
Biochemical Pharmacology published findings related to mice that were fed a high fructose high fat diet. The mice that had their diet enhanced with CoQ10 showed decreased levels of inflammatory and metabolic stress markers in their livers when compared to those that were strictly provided the high fructose high fat diet. The supplement did not seem to have any effect on obesity levels or the levels of oxidised fat in other tissues."
Friday, November 20, 2009
Paper Chase: Discovery of fat gene in mice may help humans
"A 15-page research report suggests Stuart Little may one day want to toss his calorie counter. Mice apparently have a fat gene, that when deactivated, according to a study released this fall by the University of Michigan Life Sciences Institute, keeps rodents on high-fat diets thin...
Why it matters
Obesity and Type II diabetes are on the rise in America, and are a growing problem in children and adolescents. If a gene similarly linked to obesity is identified in humans, it could lead to the development of drugs to treat and prevent excessive weight gain and health problems associated with it.
The same research team is searching for molecules that may be able to block the gene's activity.
Which offers the possibility of guiltless consumption of bon-bons."
Why it matters
Obesity and Type II diabetes are on the rise in America, and are a growing problem in children and adolescents. If a gene similarly linked to obesity is identified in humans, it could lead to the development of drugs to treat and prevent excessive weight gain and health problems associated with it.
The same research team is searching for molecules that may be able to block the gene's activity.
Which offers the possibility of guiltless consumption of bon-bons."
Thursday, November 12, 2009
Yoghurt story 'hard to swallow'
"A headline in today’s Daily Mail stated: 'Yoghurt drinks could beat bugs that pile the weight on.' It said scientists have shown that 'bugs that live in our stomachs could be causing us to get fat.' The newspaper said the research could lead to probiotic yoghurts that can combat weight gain.
The newspaper’s claim about probiotic yoghurts is misleading. In fact, the study examined the effect of a change in diet on gut flora (micro organisms found in the gut) and weight in mice...
A Western diet caused mice to gain weight and changed the microbes in their gut. Transplanting the gut flora from these mice to healthy mice led to significant weight gain compared with mice that received gut flora from mice on a non-Western diet, even though there was no increase in food consumption...
The study did not examine the effects of yoghurt or other probiotics on weight, as some news reports imply. Nor does it suggest that a probiotic yoghurt will soon be available that can aid weight loss. This extrapolation of the results is likely to have been based on the finding that a Western diet alters the microbial constituents of the gut. Researchers found that when the mice’s diet was changed from a low-fat diet to a Western-style high-fat, high-sugar diet, the component bacteria in their gut changed quickly and considerably. Stating that a probiotic yoghurt could 'combat weight gain', (sic) and including a picture of a normal yoghurt drink next to the article, could mislead people."
The newspaper’s claim about probiotic yoghurts is misleading. In fact, the study examined the effect of a change in diet on gut flora (micro organisms found in the gut) and weight in mice...
A Western diet caused mice to gain weight and changed the microbes in their gut. Transplanting the gut flora from these mice to healthy mice led to significant weight gain compared with mice that received gut flora from mice on a non-Western diet, even though there was no increase in food consumption...
The study did not examine the effects of yoghurt or other probiotics on weight, as some news reports imply. Nor does it suggest that a probiotic yoghurt will soon be available that can aid weight loss. This extrapolation of the results is likely to have been based on the finding that a Western diet alters the microbial constituents of the gut. Researchers found that when the mice’s diet was changed from a low-fat diet to a Western-style high-fat, high-sugar diet, the component bacteria in their gut changed quickly and considerably. Stating that a probiotic yoghurt could 'combat weight gain', (sic) and including a picture of a normal yoghurt drink next to the article, could mislead people."
Connections Between Circadian And Metabolic Systems Described
"A paper by University of Notre Dame biologist Giles Duffield and a team of researchers offers new insights into a gene that plays a key role in modulating the body's Circadian system and may also simultaneously modulate its metabolic system. The relationship between circadian and metabolic systems the researchers describe could have important implications for understanding the higher incidence of cardiovascular disease, obesity and diabetes among shift workers...
Not only did the knockout mice have abnormal time-of-day specific changes in the pattern of gene activity, they also exhibited profound physiological changes. The mutant mice were lean, had smaller quantities of white fat stored in their abdomen and far less fat droplets in the liver itself."
Not only did the knockout mice have abnormal time-of-day specific changes in the pattern of gene activity, they also exhibited profound physiological changes. The mutant mice were lean, had smaller quantities of white fat stored in their abdomen and far less fat droplets in the liver itself."
Is your gut bacteria making you fat? Common microorganisms may contribute to obesity
"There are billions of microorganisms in the human gut, and according to a recent study, they may be triggers of obesity.
A study published in Science Transnational Medicine indicates that when these common microorganisms encounter a Westernized diet high in carbohydrates and sugar, the microbial environment shifts and results in weight gain.
According to HealthDay, researchers at the Center for Genome Sciences at Washington University School of Medicine in St. Louis observed the microbial changes in the guts of mice. They started with mice who, by way of genetic manipulation, had no bacteria in the gut. They then transplanted human microbes into the mice.
'When we switched these humanized animals [from a low-fat] to a junk-food diet, high in fat with lots of simple sugars, the structure of the microbial community changed dramatically and very rapidly,' study senior author Dr. Jeffrey I. Gordon told HealthDay Reporter. 'These mice also became obese on Western diets.'
Because the human body is made up of 10 times more microbial cells than human cells, researchers believe it’s vital to know how the food we eat affects microbial activity.
While it would be easy to blame the mice’s weight gain on the high-fat diet, scientists also transplanted microorganisms in several mice and fed them a low-fat diet, but yielded the same results...
Perhaps the most vital conclusion out of this study, however, is that there is a direct correlation between dietary habits and microbial activity that may lead to new treatments for obesity."
A study published in Science Transnational Medicine indicates that when these common microorganisms encounter a Westernized diet high in carbohydrates and sugar, the microbial environment shifts and results in weight gain.
According to HealthDay, researchers at the Center for Genome Sciences at Washington University School of Medicine in St. Louis observed the microbial changes in the guts of mice. They started with mice who, by way of genetic manipulation, had no bacteria in the gut. They then transplanted human microbes into the mice.
'When we switched these humanized animals [from a low-fat] to a junk-food diet, high in fat with lots of simple sugars, the structure of the microbial community changed dramatically and very rapidly,' study senior author Dr. Jeffrey I. Gordon told HealthDay Reporter. 'These mice also became obese on Western diets.'
Because the human body is made up of 10 times more microbial cells than human cells, researchers believe it’s vital to know how the food we eat affects microbial activity.
While it would be easy to blame the mice’s weight gain on the high-fat diet, scientists also transplanted microorganisms in several mice and fed them a low-fat diet, but yielded the same results...
Perhaps the most vital conclusion out of this study, however, is that there is a direct correlation between dietary habits and microbial activity that may lead to new treatments for obesity."
Tuesday, November 10, 2009
Brown fat cells provide hope for obesity research
"Not all fat cells mean weight gain.
National researchers in cell biology have identified proteins that turn normal skin cells into brown fat cells, which use energy to generate heat.
'Energy only gets burned when your heart beats or your muscles walk up a flight of stairs or when you breathe,' said Clay Semenkovich, chief of the division of endocrinology, metabolism and lipid research at the Washington University School of Medicine.
Brown fat cells do not store energy. They burn it without carrying out a function, such as beating the heart or walking, Semenkovich said.
Until recently, scientists believed that only animals and human babies had brown fat cells. But researchers discovered brown fat cells in adults when PET scans showed higher rates of glucose metabolism in patients who had been waiting in cold waiting rooms at their doctors’ offices.
Brown fat evolved to help people and animals in cold environments stay warm, Semenkovich said.
“People were freezing in the waiting rooms, and they were actually turning on brown fat,” he said.
The presence of brown fat cells in human adults carries implications for obesity research.
'People who are overweight have much less active brown fat,' Semenkovich said.
Researchers at Harvard engineered skin cells from mice and humans to become brown fat. This technology requires further research, though, before scientists can test it on humans.
'There’s always a disadvantage to tricking the body into doing things that it probably should not do,' Semenkovich said.
With brown fat, that disadvantage stems from the heat that the cells release. The excess heat could lead to dangerous and possibly deadly fevers in humans."
National researchers in cell biology have identified proteins that turn normal skin cells into brown fat cells, which use energy to generate heat.
'Energy only gets burned when your heart beats or your muscles walk up a flight of stairs or when you breathe,' said Clay Semenkovich, chief of the division of endocrinology, metabolism and lipid research at the Washington University School of Medicine.
Brown fat cells do not store energy. They burn it without carrying out a function, such as beating the heart or walking, Semenkovich said.
Until recently, scientists believed that only animals and human babies had brown fat cells. But researchers discovered brown fat cells in adults when PET scans showed higher rates of glucose metabolism in patients who had been waiting in cold waiting rooms at their doctors’ offices.
Brown fat evolved to help people and animals in cold environments stay warm, Semenkovich said.
“People were freezing in the waiting rooms, and they were actually turning on brown fat,” he said.
The presence of brown fat cells in human adults carries implications for obesity research.
'People who are overweight have much less active brown fat,' Semenkovich said.
Researchers at Harvard engineered skin cells from mice and humans to become brown fat. This technology requires further research, though, before scientists can test it on humans.
'There’s always a disadvantage to tricking the body into doing things that it probably should not do,' Semenkovich said.
With brown fat, that disadvantage stems from the heat that the cells release. The excess heat could lead to dangerous and possibly deadly fevers in humans."
Brain link tips the scales
"BALWYN professor Michael Cowley has some welcome news for those struggling to lose weight - willpower alone is not the answer.
Prof Cowley has been awarded the 2009 Science Minister’s Prize for Life Scientist of the Year for his research into understanding metabolism and obesity.
The Monash University Department of Physiology professor has spent the past 10 years researching the complex issue of how people’s brains control their metabolism.
'There are good metabolic reasons why we struggle to lose weight,' Prof Cowley said.'“It’s not just about willpower. For some of us, compulsive food consumption mirrors drug addiction.'
Working with mice and monkeys, Prof Cowley identified neurons in the brain that responded to leptin, a hormone that helps regulate body weight.
He found leptin activated neurons that suppressed weight, and inhibited those increasing it."
Prof Cowley has been awarded the 2009 Science Minister’s Prize for Life Scientist of the Year for his research into understanding metabolism and obesity.
The Monash University Department of Physiology professor has spent the past 10 years researching the complex issue of how people’s brains control their metabolism.
'There are good metabolic reasons why we struggle to lose weight,' Prof Cowley said.'“It’s not just about willpower. For some of us, compulsive food consumption mirrors drug addiction.'
Working with mice and monkeys, Prof Cowley identified neurons in the brain that responded to leptin, a hormone that helps regulate body weight.
He found leptin activated neurons that suppressed weight, and inhibited those increasing it."
Thursday, November 05, 2009
Bionovo Announces Third Quarter 2009 Highlights and Financial Results
"-- The Company presented the results of a study on the effects of two plant-derived, tissue-selective estrogen receptor alpha (ERa) modulators (TSERaM) on menopausal obesity at the 20th Annual Meeting of the North American Menopause Society. In this study, plant-derived TSERaMs,like estrogens, were shown to reduce body fat in mice, but while estrogens also caused cell proliferation in the mammary gland and uterus, the plant-derived TSERaMs did not elicit these potentially cancer-causing side effects. These results suggest that the development of botanically-derived, tissue-selective ERa modulators could result in a safer alternative for the treatment of menopausal weight gain, a condition that can lead to the development of metabolic syndrome, a combination of risk factors for cardiovascular disease and diabetes."
Tuesday, November 03, 2009
‘Slimming gene’ that regulates body fat identified
"Scientists at the University of Bonn have identified a gene in fruit flies that controls the metabolism of fat.
The researchers called the gene ’schlank’ (German for ’slim’).
According to them, the discovery could help in developing new medicines to fight obesity as mammals also carry a group of genes that are structurally very similar to ’schlank’.
The larvae in which this gene is defective have been found to lose their entire fat reserves.
According to Professor Michael Hoch from the University of Bonn, ‘in extreme cases the defect can even lead to death.’
The study showed that the gene contains the instructions of what is known as ceramide synthase. Ceramides serve as raw materials for the gauzy membranes that enclose all of the cells in the body.
Moreover, schlank also has a regulatory function. It promotes lipid synthesis and at the same time inhibits the mobilisation of fat from the fat reserves.
This gene is striking similar to Lass genes from mice that partially compensate for the defect schlank gene in mutant flies."
The researchers called the gene ’schlank’ (German for ’slim’).
According to them, the discovery could help in developing new medicines to fight obesity as mammals also carry a group of genes that are structurally very similar to ’schlank’.
The larvae in which this gene is defective have been found to lose their entire fat reserves.
According to Professor Michael Hoch from the University of Bonn, ‘in extreme cases the defect can even lead to death.’
The study showed that the gene contains the instructions of what is known as ceramide synthase. Ceramides serve as raw materials for the gauzy membranes that enclose all of the cells in the body.
Moreover, schlank also has a regulatory function. It promotes lipid synthesis and at the same time inhibits the mobilisation of fat from the fat reserves.
This gene is striking similar to Lass genes from mice that partially compensate for the defect schlank gene in mutant flies."
How saturated fatty acids 'anger' the immune system (and how to stop them)
"Researchers have new evidence to explain how saturated fatty acids, which soar in those who are obese, can lead the immune system to respond in ways that add up to chronic, low-grade inflammation. The new results could lead to treatments designed to curb that inflammatory state, and the insulin resistance and type 2 diabetes that come with it.
One key, according to the report in the November Cell Metabolism, a Cell Press publication, is an immune receptor (called Toll-like receptor 4 or Tlr4) at the surface of blood cells, including a particularly 'angry' class of macrophages known to pump out toxic molecules and spur inflammation. It now appears that fatty acids may in essence 'hijack' those immune cells via Tlr4...
The researchers showed in another Cell Metabolism report last year that a 'genetic trick' designed to kill off the offending macrophages, which are distinguished by a CD11c marker, could reverse insulin resistance in obese mice...
They say that drugs aimed at Tlr4 have already been developed, and the idea that those drugs may hold promise in fighting insulin resistance and type 2 diabetes is one Olefsky's team is now exploring in detail in the mice."
One key, according to the report in the November Cell Metabolism, a Cell Press publication, is an immune receptor (called Toll-like receptor 4 or Tlr4) at the surface of blood cells, including a particularly 'angry' class of macrophages known to pump out toxic molecules and spur inflammation. It now appears that fatty acids may in essence 'hijack' those immune cells via Tlr4...
The researchers showed in another Cell Metabolism report last year that a 'genetic trick' designed to kill off the offending macrophages, which are distinguished by a CD11c marker, could reverse insulin resistance in obese mice...
They say that drugs aimed at Tlr4 have already been developed, and the idea that those drugs may hold promise in fighting insulin resistance and type 2 diabetes is one Olefsky's team is now exploring in detail in the mice."
UNMC Study Yields Clues to Cell Metabolism, Obesity
"A University of Nebraska Medical Center research study could provide new clues on cell metabolism including how energy is regulated and used. The findings, published as the cover story in the latest issue of Cell Metabolism, show that mice are obese and insulin resistant when they lack a gene that interacts with, and controls, enzymes that regulate a cell’s energy level."
Monday, November 02, 2009
A scramble to harness the metabolic power of brown fat
"Americans spend millions each year searching for the right diet or exercise program -- all in an effort to shed some fat. But there's one type of fat that most would probably like to hold on to: brown fat.
Instead of storing excess energy from food in lumps and bumps throughout the body -- like its well-known sister, white fat -- brown fat helps burn incoming calories.
Because its primary purpose is temperature regulation, brown fat cells are jam-packed with mitochondria, the powerhouses of cells. This mitochondria-heavy design is well-suited to use high quantities of sugar, the body's fuel, and then release that energy in the form of heat.
This mechanism enables small and hibernating mammals, who can't shiver, to stay warm in cold temperatures. And it enables newborn humans, who have yet to develop layers of white fat, to stay warm after exiting the stable confines of the womb.
Until recently, only these two types of creatures were thought to even have brown fat.
Now researchers have found that adults don't, in fact, lose all of their brown fat to the creeping ubiquitousness of white fat; with that finding, they've launched a scramble to discover how the substance's fat-burning abilities could be harnessed for weight loss.
If brown fat is unleashed, it could potentially "tickle" the metabolism enough to make weight loss easier and more manageable, said Sven Enerback, a researcher at the University of Gothenburg in Sweden and one of the scientists who discovered that brown fat persists in adults. As is, once a person reduces his or her starting weight, the body begins to compensate for the loss by getting better gas mileage -- that is, burning fewer calories.
Enerback calculates that inserting only 50 to 100 grams of activated brown fat into a person could significantly increase their energy metabolism and eliminate 10 pounds of white fat a year.
However, these gains in metabolic rate can be achieved only if the brown fat is active. "When heat is not needed, the burner is off -- so we need to find good ways to activate it safely," he said.
The role of cold
Researchers are exploring various avenues through which to do this. It's possible cold temperatures may play a role.
Already they've learned in experiments exposing a variety of people to cold temperatures that healthy people tend to have more active brown fat than their less healthy, older or more overweight counterparts, said Dr. Aaron Cypess of the Joslin Diabetes Center in Boston. But researchers are not sure whether the brown fat helped lead to better health or whether people in better health have more brown fat. Further investigation will need to determine whether brown fat actually plays a protective role against obesity.
"First, we need to know the significance of brown fat function in human adults -- we can look at how to increase brown fat -- but first we need to understand it more," said Wouter van Marken Lichtenbelt, a professor of physiology at Maastricht University in the Netherlands and a co-discoverer of brown fat in adults.
Recently, a team of researchers led by Dr. Bruce Spiegelman, a professor of cell biology at the Dana-Farber Cancer Institute in Boston, was able to increase brown fat stores in mice by turning immature muscle cells into brown fat cells, then transplanting these cells into adult mice."
Instead of storing excess energy from food in lumps and bumps throughout the body -- like its well-known sister, white fat -- brown fat helps burn incoming calories.
Because its primary purpose is temperature regulation, brown fat cells are jam-packed with mitochondria, the powerhouses of cells. This mitochondria-heavy design is well-suited to use high quantities of sugar, the body's fuel, and then release that energy in the form of heat.
This mechanism enables small and hibernating mammals, who can't shiver, to stay warm in cold temperatures. And it enables newborn humans, who have yet to develop layers of white fat, to stay warm after exiting the stable confines of the womb.
Until recently, only these two types of creatures were thought to even have brown fat.
Now researchers have found that adults don't, in fact, lose all of their brown fat to the creeping ubiquitousness of white fat; with that finding, they've launched a scramble to discover how the substance's fat-burning abilities could be harnessed for weight loss.
If brown fat is unleashed, it could potentially "tickle" the metabolism enough to make weight loss easier and more manageable, said Sven Enerback, a researcher at the University of Gothenburg in Sweden and one of the scientists who discovered that brown fat persists in adults. As is, once a person reduces his or her starting weight, the body begins to compensate for the loss by getting better gas mileage -- that is, burning fewer calories.
Enerback calculates that inserting only 50 to 100 grams of activated brown fat into a person could significantly increase their energy metabolism and eliminate 10 pounds of white fat a year.
However, these gains in metabolic rate can be achieved only if the brown fat is active. "When heat is not needed, the burner is off -- so we need to find good ways to activate it safely," he said.
The role of cold
Researchers are exploring various avenues through which to do this. It's possible cold temperatures may play a role.
Already they've learned in experiments exposing a variety of people to cold temperatures that healthy people tend to have more active brown fat than their less healthy, older or more overweight counterparts, said Dr. Aaron Cypess of the Joslin Diabetes Center in Boston. But researchers are not sure whether the brown fat helped lead to better health or whether people in better health have more brown fat. Further investigation will need to determine whether brown fat actually plays a protective role against obesity.
"First, we need to know the significance of brown fat function in human adults -- we can look at how to increase brown fat -- but first we need to understand it more," said Wouter van Marken Lichtenbelt, a professor of physiology at Maastricht University in the Netherlands and a co-discoverer of brown fat in adults.
Recently, a team of researchers led by Dr. Bruce Spiegelman, a professor of cell biology at the Dana-Farber Cancer Institute in Boston, was able to increase brown fat stores in mice by turning immature muscle cells into brown fat cells, then transplanting these cells into adult mice."
Scientists discover gene that controls the metabolism of fat
"Scientists at the University of Bonn have discovered a previously unknown fruit fly gene that controls the metabolism of fat. Larvae in which this gene is defective lose their entire fat reserves. Therefore the researchers called the gene 'schlank' (German for 'slim'). Mammals carry a group of genes that are structurally very similar to 'schlank'. They possibly take on a similar function in the energy metabolism. The scientists therefore have hopes in new medicines with which obesity could be fought. Their research bas been published in 'The EMBO Journal' (doi: 10.1038/emboj.2009.305)...
Mouse gene saves fly larvae
There is a chance that this is not only the case in fruit flies. Humans also produce ceramide synthases however not just one as Drosophila does but rather as many as six different ones. For this purpose humans rely on a group of genes so-called Lass genes. Ceramide synthases are extremely important for animals. Mutations in the corresponding genes lead to severe metabolic disorders and to malfunctions of organ systems. That is why our Lass genes look surprisingly similar to the schlank gene of fruit flies.
This resemblance is so striking that Lass genes from mice can partially compensate for the defect schlank gene in mutant flies. 'We introduced a mouse Lass gene in mutant Drosophila larvae,' Michael Hoch says. 'Normally the larvae died immediately after hatching. Thanks to the Lass gene they resumed building up body fat and survived until the next development stage.'"
Mouse gene saves fly larvae
There is a chance that this is not only the case in fruit flies. Humans also produce ceramide synthases however not just one as Drosophila does but rather as many as six different ones. For this purpose humans rely on a group of genes so-called Lass genes. Ceramide synthases are extremely important for animals. Mutations in the corresponding genes lead to severe metabolic disorders and to malfunctions of organ systems. That is why our Lass genes look surprisingly similar to the schlank gene of fruit flies.
This resemblance is so striking that Lass genes from mice can partially compensate for the defect schlank gene in mutant flies. 'We introduced a mouse Lass gene in mutant Drosophila larvae,' Michael Hoch says. 'Normally the larvae died immediately after hatching. Thanks to the Lass gene they resumed building up body fat and survived until the next development stage.'"
The Chemical Cause of Fat
"There is a new and growing scientific explanation for obesityand obesity-related disorders, like cardiovascular disease, hypertension and type 2 diabetes, which does not involve living in a couch-potato culture and stuffing yourself with more calories than you can burn.
Dr. Bruce Blumberg, Professor for the Department of Pharmaceutical Sciences at UC Irvine, and his colleagues have determined thatobesogens, especially those that are environmental contaminants, are a possible explanation for the worldwide epidemic...
Connie Chow, a fourth-year biological sciences major, and Tiffany Kieu, a fourth-year developmental and cell biology major, are the only undergraduates currently working on the project. Their work is in submission to be reviewed for publication in a journal...
Blumberg and his colleagues have done a previous study showing that pregnant mice treated with TBT will have pup that become fatter when they grow up. Kieu assisted her post-doctoral supervisor, Severine Kirchner, with examining how prenatal exposure to TBT in the womb can later effect the development and function of adipose tissue in young mice. In this research, Kieu contributed most extensively to the RNA analysis"
Dr. Bruce Blumberg, Professor for the Department of Pharmaceutical Sciences at UC Irvine, and his colleagues have determined thatobesogens, especially those that are environmental contaminants, are a possible explanation for the worldwide epidemic...
Connie Chow, a fourth-year biological sciences major, and Tiffany Kieu, a fourth-year developmental and cell biology major, are the only undergraduates currently working on the project. Their work is in submission to be reviewed for publication in a journal...
Blumberg and his colleagues have done a previous study showing that pregnant mice treated with TBT will have pup that become fatter when they grow up. Kieu assisted her post-doctoral supervisor, Severine Kirchner, with examining how prenatal exposure to TBT in the womb can later effect the development and function of adipose tissue in young mice. In this research, Kieu contributed most extensively to the RNA analysis"
Mice and Men
"The price tag on a mouse bred at Jackson Laboratory in Bar Harbor runs anywhere from $11 to $300. The lower fee buys a basic, all-purpose mouse, fit for a variety of scientific experiments, while a bit more gets a custom rodent with a disease of the customer’s choice. The mice can be ordered online, in bulk, and packed up in temperature-controlled tractor trailers for delivery within days. While supplies last, take 25% off selected products. Just add shipping and handling.
All this may sound rather commercial for a nonprofit, world-renowned genetics research institution. But selling mice has been part of Jackson Lab’s mission ever since the 1929 stock market crash threatened its founding 80 years ago. Today, the lab houses and distributes more than 4,000 different strains of mice — ideal as a research model for their genetic similarity to humans — and is recognized worldwide for its diverse, reliable stock. It is not the only place to buy laboratory mice, but its rodents are indispensable to scientists across the globe researching how and why we get sick...
The research driving personalized medicine is happening both in-house at Jackson Lab and at the pharmaceutical companies and biotechs the lab supplies with its mice. The lab employs 218 researchers working to understand and better treat diseases including cancer, osteoporosis, AIDS, obesity and glaucoma. Last year, the lab distributed 2.5 million mice — which are genetically pure through inbreeding — to 16,000 investigators in 60 countries. Many of them couldn’t do similar testing otherwise, Woychik says. 'There are major pharmaceutical companies whose R&D efforts are dependent on the resources that we create here. We’re doing experiments in mice that will make it safer to bring a drug into clinical trials.'...
Jackson Lab also provides mice that can accept human tissue, allowing researchers to test the efficacy of new drugs on as human-like a subject as possible. Hospitals provide the lab with human tumors that can be inserted into the mice, furthering research into cancer drugs, as well treatments for illnesses including as obesity and diabetes. 'You’re one step closer to really studying the human disease in life, not in a petri dish,' Hewett says."
All this may sound rather commercial for a nonprofit, world-renowned genetics research institution. But selling mice has been part of Jackson Lab’s mission ever since the 1929 stock market crash threatened its founding 80 years ago. Today, the lab houses and distributes more than 4,000 different strains of mice — ideal as a research model for their genetic similarity to humans — and is recognized worldwide for its diverse, reliable stock. It is not the only place to buy laboratory mice, but its rodents are indispensable to scientists across the globe researching how and why we get sick...
The research driving personalized medicine is happening both in-house at Jackson Lab and at the pharmaceutical companies and biotechs the lab supplies with its mice. The lab employs 218 researchers working to understand and better treat diseases including cancer, osteoporosis, AIDS, obesity and glaucoma. Last year, the lab distributed 2.5 million mice — which are genetically pure through inbreeding — to 16,000 investigators in 60 countries. Many of them couldn’t do similar testing otherwise, Woychik says. 'There are major pharmaceutical companies whose R&D efforts are dependent on the resources that we create here. We’re doing experiments in mice that will make it safer to bring a drug into clinical trials.'...
Jackson Lab also provides mice that can accept human tissue, allowing researchers to test the efficacy of new drugs on as human-like a subject as possible. Hospitals provide the lab with human tumors that can be inserted into the mice, furthering research into cancer drugs, as well treatments for illnesses including as obesity and diabetes. 'You’re one step closer to really studying the human disease in life, not in a petri dish,' Hewett says."
Wednesday, October 28, 2009
Junk food as 'addictive as drugs'
"A diet of burgers, chips, sausages and cake will programme your brain into craving even more foods that are high in sugar, salt and fat, according to new research.
Over the years these junk foods can become a substitute for happiness and will lead bingers to become addicted.
Dr Paul Kenny, a neuroscientist, carried out the research which shows how dangerous high fat and high sugar foods can be to our health.
'You lose control. It’s the hallmark of addiction,' he said.
The researchers believe it is one of the first studies to suggest brains may react in the same way to junk food as they do to drugs...
Dr Kenny, who began his research at Guy’s Hospital, London, but now works at Florida’s Scripps Research Institute, divided rats into three groups for his research, due to be published in teh US soon.
One got normal amounts of healthy food to eat. Another lot was given restricted amounts of junk food and the third group was given unlimited amounts of junk, including cheesecake, fatty meat products, and cheap sponge cakes and chocolate snacks.
There were no adverse effects on the first two groups, but the rats who ate as much junk food as they wanted quickly became very fat and started bingeing. (sic)
When researchers electronically stimulated the part of the brain that feels pleasure, they found that the rats on unlimited junk food needed more and more stimulation to register the same level of pleasure as the animals on healthier diets."
Over the years these junk foods can become a substitute for happiness and will lead bingers to become addicted.
Dr Paul Kenny, a neuroscientist, carried out the research which shows how dangerous high fat and high sugar foods can be to our health.
'You lose control. It’s the hallmark of addiction,' he said.
The researchers believe it is one of the first studies to suggest brains may react in the same way to junk food as they do to drugs...
Dr Kenny, who began his research at Guy’s Hospital, London, but now works at Florida’s Scripps Research Institute, divided rats into three groups for his research, due to be published in teh US soon.
One got normal amounts of healthy food to eat. Another lot was given restricted amounts of junk food and the third group was given unlimited amounts of junk, including cheesecake, fatty meat products, and cheap sponge cakes and chocolate snacks.
There were no adverse effects on the first two groups, but the rats who ate as much junk food as they wanted quickly became very fat and started bingeing. (sic)
When researchers electronically stimulated the part of the brain that feels pleasure, they found that the rats on unlimited junk food needed more and more stimulation to register the same level of pleasure as the animals on healthier diets."
Analysis of knockout mice suggests a role for VGF in the control of fat storage and energy expenditure
"Previous studies of mixed background mice have demonstrated that targeted deletion of Vgf produces a lean, hypermetabolic mouse that is resistant to diet-, lesion-, and genetically-induced obesity. To investigate potential mechanism(s) and site(s) of action of VGF, a neuronal and endocrine secreted protein and neuropeptide precursor, we further analyzed the metabolic phenotypes of two independent VGF knockout lines on C57Bl6 backgrounds...
Conclusions: We propose that VGF and/or VGF-derived peptides modulate sympathetic outflow pathways to regulate fat storage and energy expenditure."
Conclusions: We propose that VGF and/or VGF-derived peptides modulate sympathetic outflow pathways to regulate fat storage and energy expenditure."
Tuesday, October 27, 2009
Maternal High-Fat Diet Has Serious Implications For Brain Development Of Offspring, Mouse Study Finds
"Feeding high-fat food to pregnant mice can affect their pups' brain development in ways that may cause them to be more vulnerable to obesity and to engage in addictive-like behaviors in adulthood, a new study has found.
The research was presented at Neuroscience 2009, the annual meeting of the Society for Neuroscience and the world's largest source of emerging news about brain science and health.
'We discovered that pups born to mothers fed a high-fat diet during pregnancy and lactation had significant changes in their brain chemistry, with dramatic differences in dopamine- and opioid-related molecules,' said lead author Teresa Reyes, PhD, of the University of Pennsylvania.
These changes may partially explain the differences in behavior observed in these pups compared with ones from normal pregnancies, Reyes added. The pups born to mothers fed a high-fat diet showed a greater preference for a sugar solution and a greater physical response to cocaine than did pups born to mothers fed a standard diet.
The study's findings may have implications for humans. Almost two-thirds of Americans are overweight and one in three is obese, according to government health surveys. Women who are obese currently account for between 20 and 35 percent of all pregnancies in the United States. 'The potential long-term effects of maternal obesity on the brains and behavior of offspring are just beginning to be understood,' Reyes said."
The research was presented at Neuroscience 2009, the annual meeting of the Society for Neuroscience and the world's largest source of emerging news about brain science and health.
'We discovered that pups born to mothers fed a high-fat diet during pregnancy and lactation had significant changes in their brain chemistry, with dramatic differences in dopamine- and opioid-related molecules,' said lead author Teresa Reyes, PhD, of the University of Pennsylvania.
These changes may partially explain the differences in behavior observed in these pups compared with ones from normal pregnancies, Reyes added. The pups born to mothers fed a high-fat diet showed a greater preference for a sugar solution and a greater physical response to cocaine than did pups born to mothers fed a standard diet.
The study's findings may have implications for humans. Almost two-thirds of Americans are overweight and one in three is obese, according to government health surveys. Women who are obese currently account for between 20 and 35 percent of all pregnancies in the United States. 'The potential long-term effects of maternal obesity on the brains and behavior of offspring are just beginning to be understood,' Reyes said."
Maternal Mice Fed High-Fat Diet Produce Larger Pups
"Could a woman's food choices during pregnancy affect not only the size and health of her children, but of her grandchildren? Yes, suggests a new study in mice presented at Neuroscience 2009, the annual meeting of the Society for Neuroscience and the world's largest source of emerging news about brain science and health.
University of Pennsylvania researchers found that pregnant mice fed a high-fat diet produce pups that are longer, weigh more, and have reduced insulin sensitivity -- factors that indicate a risk for obesity and diabetes. Interestingly, despite the lack of further high-fat diet exposure, the traits of increased body length and insulin insensitivity persisted into the second generation.
Subsequent investigation found that the changes in gene expression responsible for alterations in body length and insulin insensitivity were sex-dependent. Only female offspring exhibited evidence of altered programming of the growth hormone axis, a gene pathway that controls overall growth and metabolism.
This work adds to the growing body of research in epigenetics, the study of heritable alterations in gene expression that act independently of changes in DNA sequence. Until very recently, scientists believed that our genes were the sole carrier of hereditary information. However, in addition to inheriting genes from our parents, we can also inherit their epigenetic 'switches' that turn our genes on or off. These switches can be flipped by our environments and experiences to help us adapt to challenges put before us, and can be passed from generation to generation."
University of Pennsylvania researchers found that pregnant mice fed a high-fat diet produce pups that are longer, weigh more, and have reduced insulin sensitivity -- factors that indicate a risk for obesity and diabetes. Interestingly, despite the lack of further high-fat diet exposure, the traits of increased body length and insulin insensitivity persisted into the second generation.
Subsequent investigation found that the changes in gene expression responsible for alterations in body length and insulin insensitivity were sex-dependent. Only female offspring exhibited evidence of altered programming of the growth hormone axis, a gene pathway that controls overall growth and metabolism.
This work adds to the growing body of research in epigenetics, the study of heritable alterations in gene expression that act independently of changes in DNA sequence. Until very recently, scientists believed that our genes were the sole carrier of hereditary information. However, in addition to inheriting genes from our parents, we can also inherit their epigenetic 'switches' that turn our genes on or off. These switches can be flipped by our environments and experiences to help us adapt to challenges put before us, and can be passed from generation to generation."
Monday, October 26, 2009
Halsa Pharmaceuticals Announces ZAG Demonstrates Weight Loss, Rise in Temperature and Reduction of Diabetes Symptoms in Preclinical Studies at Obesity
"Suggests Increase in Energy Expenditure and Potential as Treatment for Obesity and Type 2 Diabetes
HOUSTON--(Business Wire)--
Houston-based Halsa Pharmaceuticals, Inc., a biotechnology company developing therapeutics for the treatment of obesity, diabetes, cachexia and other metabolic diseases, today announced results from preclinical studies demonstrating that recombinant human Zinc-α2-glycoprotein (ZAG) induced a progressive loss of body weight in mice of 3.5g in five days, together with a rise in temperature of 0.4°C, suggesting an increase in energy expenditure. In addition, ZAG produced a normalization of the diabetic glucose tolerance curve after three days of treatment, suggesting that ZAG may have a therapeutic application in the treatment of obesity and Type 2 diabetes. The results from this study were presented at Obesity 2009, the 27th Annual Scientific Meeting of The Obesity Society, one of the largest scientific conferences in the field of obesity, being held in Washington, D.C. October 24-28...
Summary Results:
* ZAG induced a progressive loss of body weight in mice of 3.5g in five days, together with a rise in temperature of 0.4°C."
HOUSTON--(Business Wire)--
Houston-based Halsa Pharmaceuticals, Inc., a biotechnology company developing therapeutics for the treatment of obesity, diabetes, cachexia and other metabolic diseases, today announced results from preclinical studies demonstrating that recombinant human Zinc-α2-glycoprotein (ZAG) induced a progressive loss of body weight in mice of 3.5g in five days, together with a rise in temperature of 0.4°C, suggesting an increase in energy expenditure. In addition, ZAG produced a normalization of the diabetic glucose tolerance curve after three days of treatment, suggesting that ZAG may have a therapeutic application in the treatment of obesity and Type 2 diabetes. The results from this study were presented at Obesity 2009, the 27th Annual Scientific Meeting of The Obesity Society, one of the largest scientific conferences in the field of obesity, being held in Washington, D.C. October 24-28...
Summary Results:
* ZAG induced a progressive loss of body weight in mice of 3.5g in five days, together with a rise in temperature of 0.4°C."
Study Says Blueberries May Help Maintain Weight, Prevent Diabetes
"The extract from North American lowbush blueberries biotransformed with bacteria from the skin of the fruit has shown promising results in tests against obesity and high blood sugar, according to new research.
Scientists from the Universite de Montreal, the Institut Armand-Frappier and the Universite de Moncton tested the blueberry juice on mice prone to obesity, insulin resistance, diabetes and hypertension, and discovered that the extract reduced their food intake and led to lower body weight.
They concluded that the biotransformed blueberry juice holds great therapeutic promise because it seems to decrease hyperglycemia by up to 35 percent and can protect young pre-diabetic animals from developing these metabolic conditions in the first place."
Scientists from the Universite de Montreal, the Institut Armand-Frappier and the Universite de Moncton tested the blueberry juice on mice prone to obesity, insulin resistance, diabetes and hypertension, and discovered that the extract reduced their food intake and led to lower body weight.
They concluded that the biotransformed blueberry juice holds great therapeutic promise because it seems to decrease hyperglycemia by up to 35 percent and can protect young pre-diabetic animals from developing these metabolic conditions in the first place."
Saturday, October 24, 2009
Scientists seek origins of obesity in the womb
"When Kathy Perusse had weight-loss surgery and shed 120 pounds, she may have done more than make her own life easier.
She went on to have two daughters, and she may have boosted their chances of avoiding becoming obese, like her two older children are.
That's the implication of research suggesting that something in an obese woman's womb can program her fetus toward becoming a fat child and adult. It's not about simply passing along genes that promote obesity; it's some sort of still-mysterious signal.
The idea has only recently entered conversations between doctors and female patients, and scientists are scrambling to track down a biological explanation. That knowledge, in turn, may provide new ways to block obesity from crossing generations.
While there's some disagreement on how important the womb signal is, 'the evidence is building and building that it is a substantial issue,' said Dr. Matthew Gillman of Harvard Medical School, who studies prevention of obesity.
Others agree. 'I think it could be a hugely significant factor,' said Robert Waterland of the Baylor College of Medicine in Houston, who studies the effect in mice."
She went on to have two daughters, and she may have boosted their chances of avoiding becoming obese, like her two older children are.
That's the implication of research suggesting that something in an obese woman's womb can program her fetus toward becoming a fat child and adult. It's not about simply passing along genes that promote obesity; it's some sort of still-mysterious signal.
The idea has only recently entered conversations between doctors and female patients, and scientists are scrambling to track down a biological explanation. That knowledge, in turn, may provide new ways to block obesity from crossing generations.
While there's some disagreement on how important the womb signal is, 'the evidence is building and building that it is a substantial issue,' said Dr. Matthew Gillman of Harvard Medical School, who studies prevention of obesity.
Others agree. 'I think it could be a hugely significant factor,' said Robert Waterland of the Baylor College of Medicine in Houston, who studies the effect in mice."
Thursday, October 22, 2009
You are what you eat
"Washington: The popular adage "you are what you eat" is literally true, according to a new research that claims a person's diet has a profound influence on his or her brain.
The findings offer insight into the neurobiological factors behind the obesity epidemic in the world.
In addition, the study exposed changes in brain chemistry due to diet and weight gain.
Obesity has been linked to rises in diabetes, stroke, and heart attacks, among other disorders, but the new research has added another dimension to understanding how obesity rates have more than doubled in the past 30 years.
The new findings show that disruptions in the sleep/wake cycle lead to weight gain, impulsivity, slower thinking, and other physiological and behavioural changes.
This could be particularly important for people who do shift work.
The study also showed that pregnant mice fed a high-fat diet produced pups that were longer, weighed more, and had reduced insulin sensitivity - factors that indicate a predisposition toward obesity and diabetes. In addition, despite no further exposure to a high-fat diet, these pups passed on those same traits to their offspring.
Feeding high-fat food to pregnant mice can affect the brain development of their offspring, causing the pups to be more vulnerable to obesity and to engaging in addictive-like behaviours in adulthood, found the researchers."
The findings offer insight into the neurobiological factors behind the obesity epidemic in the world.
In addition, the study exposed changes in brain chemistry due to diet and weight gain.
Obesity has been linked to rises in diabetes, stroke, and heart attacks, among other disorders, but the new research has added another dimension to understanding how obesity rates have more than doubled in the past 30 years.
The new findings show that disruptions in the sleep/wake cycle lead to weight gain, impulsivity, slower thinking, and other physiological and behavioural changes.
This could be particularly important for people who do shift work.
The study also showed that pregnant mice fed a high-fat diet produced pups that were longer, weighed more, and had reduced insulin sensitivity - factors that indicate a predisposition toward obesity and diabetes. In addition, despite no further exposure to a high-fat diet, these pups passed on those same traits to their offspring.
Feeding high-fat food to pregnant mice can affect the brain development of their offspring, causing the pups to be more vulnerable to obesity and to engaging in addictive-like behaviours in adulthood, found the researchers."
Monday, October 19, 2009
The Food-Energy Cellular Connection Revealed: Metabolic Master Switch Sets the Biological Clock in Body Tissues
Our body's activity levels fall and rise to the beat of our internal drums-the 24-hour cycles that govern fundamental physiological functions, from sleeping and feeding patterns to the energy available to our cells. Whereas the master clock in the brain is set by light, the pacemakers in peripheral organs are set by food availability. The underlying molecular mechanism was unknown.
Now, researchers at the Salk Institute for Biological Studies shed light on the long missing connection: A metabolic master switch, which, when thrown, allows nutrients to directly alter the rhythm of peripheral clocks.
Since the body's circadian rhythm and its metabolism are closely intertwined, the risk for metabolic disease shoots up, when they are out of sync. "Shift workers face a 100 percent increase in the risk for obesity and its consequences, such as high blood pressure, insulin resistance and an increased risk of heart attacks," says Howard Hughes Medical Investigator Ronald M. Evans, Ph.D., a professor in the Salk Institute's Gene Expression Laboratory...
Genetic inactivation of AMPK in mice blocks these effects, stabilizing CRY1 and severely disrupting peripheral clocks. In contrast, treating mice with AICAR, a synthetic drug that directly activates AMPK, reset the clock in cultured cells as well as in animals, confirming that cryptochromes act as energy sensors that allow to circadian clocks."
Now, researchers at the Salk Institute for Biological Studies shed light on the long missing connection: A metabolic master switch, which, when thrown, allows nutrients to directly alter the rhythm of peripheral clocks.
Since the body's circadian rhythm and its metabolism are closely intertwined, the risk for metabolic disease shoots up, when they are out of sync. "Shift workers face a 100 percent increase in the risk for obesity and its consequences, such as high blood pressure, insulin resistance and an increased risk of heart attacks," says Howard Hughes Medical Investigator Ronald M. Evans, Ph.D., a professor in the Salk Institute's Gene Expression Laboratory...
Genetic inactivation of AMPK in mice blocks these effects, stabilizing CRY1 and severely disrupting peripheral clocks. In contrast, treating mice with AICAR, a synthetic drug that directly activates AMPK, reset the clock in cultured cells as well as in animals, confirming that cryptochromes act as energy sensors that allow to circadian clocks."
Lard Lesson: Why Fat Lubricates Your Appetite
"Researchers have long known that the hormones leptin and insulin play key roles in appetite and food intake. In healthy people leptin, which is secreted by fat tissue, acts as a molecular measuring tape for our waistlines, quashing feelings of hunger. Insulin spikes when the pancreas gets a whiff of the blood sugar increase after a meal; once the brain detects the spike, it knows to tamp down the desire for food.
Certain foods and metabolic disorders, however, can disrupt our ability to respond appropriately to these hormonal signals. In a study published in the September issue of The Journal of Clinical Investigation, scientists report unraveling a central biochemical mechanism behind fat's effect on the mammalian brain . They found that after only three days on a diet high in saturated fat—a common ingredient in beef and cheese—the brains of rats and mice became resistant to leptin and insulin. In contrast, unsaturated fats, such as those found in olive oil, did not trigger resistance."
Certain foods and metabolic disorders, however, can disrupt our ability to respond appropriately to these hormonal signals. In a study published in the September issue of The Journal of Clinical Investigation, scientists report unraveling a central biochemical mechanism behind fat's effect on the mammalian brain . They found that after only three days on a diet high in saturated fat—a common ingredient in beef and cheese—the brains of rats and mice became resistant to leptin and insulin. In contrast, unsaturated fats, such as those found in olive oil, did not trigger resistance."
Hormone Deficiency Linked to Impaired Glucose Metabolism
"Mice deficient in a gastrointestinal hormone implicated in glucose metabolism spontaneously develop impaired glucose tolerance, insulin resistance and visceral obesity, according to a study published online Oct. 9 in Endocrinology...
The researchers found that the mice had normal levels of active glucagon-like peptide 1. By four months, the mice spontaneously developed fasting hyperglycemia, hyperinsulinemia, glucose intolerance, insulin resistance, and visceral obesity."
The researchers found that the mice had normal levels of active glucagon-like peptide 1. By four months, the mice spontaneously developed fasting hyperglycemia, hyperinsulinemia, glucose intolerance, insulin resistance, and visceral obesity."
Sunday, October 18, 2009
Obesity Cure May Lie In Converting White Fat Cells Into Their Brown Counterparts
"A recent study has proved that manipulating autophagy - a cellular process which regulates the formation and inter-conversion of white fat cells and brown fat cells in mice - could solve the problem of obesity."
Thursday, October 15, 2009
The food-energy cellular connection revealed
"Our body's activity levels fall and rise to the beat of our internal drums—the 24-hour cycles that govern fundamental physiological functions, from sleeping and feeding patterns to the energy available to our cells. Whereas the master clock in the brain is set by light, the pacemakers in peripheral organs are set by food availability. The underlying molecular mechanism was unknown.
Now, researchers at the Salk Institute for Biological Studies shed light on the long missing connection: A metabolic master switch, which, when thrown, allows nutrients to directly alter the rhythm of peripheral clocks.
Since the body's circadian rhythm and its metabolism are closely intertwined, the risk for metabolic disease shoots up, when they are out of sync. 'Shift workers face a 100 percent increase in the risk for obesity and its consequences, such as high blood pressure, insulin resistance and an increased risk of heart attacks,' says Howard Hughes Medical Investigator Ronald M. Evans, Ph.D., a professor in the Salk Institute's Gene Expression Laboratory.
The researchers' findings, which are published in the Oct. 16, 2009, issue of Science, could have far-reaching implications, from providing a better understanding how nutrition and gene expression are linked, to creating new ways to treat obesity, diabetes and other related diseases. 'It is estimated that the activity of up to 15 percent of our genes is under the direct control of biological clocks,' says Evans. 'Our work provides a conceptual way to link nutrition and energy regulation to the genome.'...
Genetic inactivation of AMPK in mice blocks these effects, stabilizing CRY1 and severely disrupting peripheral clocks. In contrast, treating mice with AICAR, a synthetic drug that directly activates AMPK, reset the clock in cultured cells as well as in animals, confirming that cryptochromes act as energy sensors that allow to circadian clocks."
Now, researchers at the Salk Institute for Biological Studies shed light on the long missing connection: A metabolic master switch, which, when thrown, allows nutrients to directly alter the rhythm of peripheral clocks.
Since the body's circadian rhythm and its metabolism are closely intertwined, the risk for metabolic disease shoots up, when they are out of sync. 'Shift workers face a 100 percent increase in the risk for obesity and its consequences, such as high blood pressure, insulin resistance and an increased risk of heart attacks,' says Howard Hughes Medical Investigator Ronald M. Evans, Ph.D., a professor in the Salk Institute's Gene Expression Laboratory.
The researchers' findings, which are published in the Oct. 16, 2009, issue of Science, could have far-reaching implications, from providing a better understanding how nutrition and gene expression are linked, to creating new ways to treat obesity, diabetes and other related diseases. 'It is estimated that the activity of up to 15 percent of our genes is under the direct control of biological clocks,' says Evans. 'Our work provides a conceptual way to link nutrition and energy regulation to the genome.'...
Genetic inactivation of AMPK in mice blocks these effects, stabilizing CRY1 and severely disrupting peripheral clocks. In contrast, treating mice with AICAR, a synthetic drug that directly activates AMPK, reset the clock in cultured cells as well as in animals, confirming that cryptochromes act as energy sensors that allow to circadian clocks."
Pain Response To Heat Reduced By Comfort Food
Choose water.
"People often eat food to feel better, but researchers have found that eating chocolate or drinking water can blunt pain, reducing a rat's response to a hot stimulus. This natural form of pain relief may help animals in the wild avoid distraction while eating scarce food, but in modern humans with readily available food, the effect may contribute to overeating and obesity."
Tuesday, October 13, 2009
Student researches obesity vaccine
"Nathan Freeman was still in high school when he joined a research team investigating possible cures for obesity.
Now a sophomore biochemistry major at USM, Freeman has continued working with the University Medical Center team every Summer for the past four years. Freeman believes that the team has made major progress developing the use of a hormone known as leptin. Secreted by fat cells, leptin is the chemical that tells your brain you are hungry. leptin is also responsible for regulating heart rate, and has effects similar to insulin for alleviating Diabetes...
Recent research by Dr. Alex da Silva of the University Medical Center showed that leptin was able to completely cure Type 2 Diabetes when given to diabetic mice."
Now a sophomore biochemistry major at USM, Freeman has continued working with the University Medical Center team every Summer for the past four years. Freeman believes that the team has made major progress developing the use of a hormone known as leptin. Secreted by fat cells, leptin is the chemical that tells your brain you are hungry. leptin is also responsible for regulating heart rate, and has effects similar to insulin for alleviating Diabetes...
Recent research by Dr. Alex da Silva of the University Medical Center showed that leptin was able to completely cure Type 2 Diabetes when given to diabetic mice."
Inhibiting the cellular process autophagy makes mice leaner
"Recent data have indicated that the more brown fat cells a person has the lower their body mass. This contrasts with what is known for white fat cells, the more white fat cells a person has the greater their body mass. It has been suggested that manipulating the development of fat cells so that they become brown fat cells rather than white fat cells might be an approach to treat obesity. However, before such an approach can be developed more needs to be learned about the mechanisms regulating the formation, expansion, and interconversion of these two cell types. New research, performed by Mark Czaja and colleagues, at Albert Einstein College of Medicine, New York, has now identified a cellular process that regulates the formation of the distinct fat cell types in mice."
Monday, October 12, 2009
Aging heart can be prevented in mice
"Factors such as high fever, anemia, lung infections, pulmonary embolism, high salt or fluid intake, overexertion, obesity, stress, and rapid heartbeat can worsen or trigger congestive heart failure in people with already weakened hearts."
" Scientists in Japan said they have uncovered evidence, based on mouse studies, that shows it may be possible to delay or prevent heart failure in humans."
Sunday, October 11, 2009
Dietary Capsaicin Reduces Obesity-induced Insulin Resistance and Hepatic Steatosis in Obese Mice Fed a High-fat Diet
"Obesity-induced inflammation contributes to the development of obesity-related metabolic disorders such as insulin resistance, type 2 diabetes, fatty liver disease, and cardiovascular disease. In this study, we investigated whether dietary capsaicin can reduce obesity-induced inflammation and metabolic disorders such as insulin resistance and hepatic steatosis. Male C57BL/6 obese mice fed a high-fat diet for 10 weeks received a supplement of 0.015% capsaicin for a further 10 weeks and were compared with unsupplemented controls...
Our data suggest that dietary capsaicin may reduce obesity-induced glucose intolerance by not only suppressing inflammatory responses but also enhancing fatty acid oxidation in adipose tissue and/or liver, both of which are important peripheral tissues affecting insulin resistance. The effects of capsaicin in adipose tissue and liver are related to its dual action on PPAR and TRPV-1 expression/activation."
Our data suggest that dietary capsaicin may reduce obesity-induced glucose intolerance by not only suppressing inflammatory responses but also enhancing fatty acid oxidation in adipose tissue and/or liver, both of which are important peripheral tissues affecting insulin resistance. The effects of capsaicin in adipose tissue and liver are related to its dual action on PPAR and TRPV-1 expression/activation."
Diet boosts mitochondrial function, has implications for humans
"Flies fed an 'anti-Atkins' low protein diet live longer because their mitochondria function better. The research, done at the Buck Institute for Age Research, shows that the molecular mechanisms responsible for the lifespan extension in the flies have important implications for human aging and diseases such as obesity, diabetes and cancer...
The study provides a significant advance in understanding the role of 4EBP, a downstream molecular target of TOR, which mediates a switch in metabolism to extend lifespan, Kapahi said. A recent study appearing in the Nature showed that feeding rapamycin (an antibiotic used to prevent the rejection of organ and bone marrow transplants) to mice inhibited TOR and extended their lifespan. The Buck Institute study implies an important role for 4EBP and mitochondrial function as excellent targets to explore their role in lifespan extension in mammals, Kapahi said."
The study provides a significant advance in understanding the role of 4EBP, a downstream molecular target of TOR, which mediates a switch in metabolism to extend lifespan, Kapahi said. A recent study appearing in the Nature showed that feeding rapamycin (an antibiotic used to prevent the rejection of organ and bone marrow transplants) to mice inhibited TOR and extended their lifespan. The Buck Institute study implies an important role for 4EBP and mitochondrial function as excellent targets to explore their role in lifespan extension in mammals, Kapahi said."
Saturday, October 10, 2009
Body Clock, Blood Sugar Control Seem Linked
"A strong link exists between the body's biological clock and blood sugar control, say U.S. researchers who conducted lab experiments on mouse and human stem cells, as well as genetically engineered mice.
'The most surprising part of our findings is that our internal biologic rhythms are embedded directly into another pathway, one that is essential to regulate metabolism,' senior author Dr. Brian Feldman, an assistant professor of pediatric endocrinology at the Stanford University School of Medicine, said in a university news release.
The researchers found that daily fluctuations in hormones called glucocorticoids synchronize the biological clock as part of the mechanism for regulating blood sugar levels. The finding may help lead to new ways to control diabetics' blood sugar levels and may improve understanding of why night-shift workers are at risk for obesity and diabetes."
'The most surprising part of our findings is that our internal biologic rhythms are embedded directly into another pathway, one that is essential to regulate metabolism,' senior author Dr. Brian Feldman, an assistant professor of pediatric endocrinology at the Stanford University School of Medicine, said in a university news release.
The researchers found that daily fluctuations in hormones called glucocorticoids synchronize the biological clock as part of the mechanism for regulating blood sugar levels. The finding may help lead to new ways to control diabetics' blood sugar levels and may improve understanding of why night-shift workers are at risk for obesity and diabetes."
Timing of meals may affect weight gain
"Mice fed a high-fat diet during their normal sleep and rest period gained significantly more weight than mice fed the same diet during their active hours, a new study shows. The finding suggests that when we eat may influence how we pack on pounds.
Many living organisms-from plants to fruit flies to humans-have internal biological clocks, or circadian rhythms, that govern our daily cycles of sleep and activity. These internal clocks are tied to cycles of light and darkness. Several recent studies have found that circadian clocks can affect metabolism in animals, suggesting that the timing of meals might influence whether incoming calories are burned or stored as fat.
To take a closer look, Dr Fred Turek, Deanna M. Arble and their colleagues at Northwestern University designed a study to search for a direct link between meal times and body weight. Their research is supported by NIH's National Institute on Aging (NIA) and National Heart, Lung and Blood Institute (NHLBI).
For 6 weeks, mice were fed a high-fat diet either during a 12-hour dark phase, when the mice are normally active, or during a 12-hour light phase, when the mice are normally resting. The mice could eat as much as they wanted during their assigned feeding periods, but the food was removed during the remaining 12 hours each day. The study was described in the 3 September 2009 advance online edition of Obesity.
The researchers found that both groups of mice had similar levels of activity and calorie consumption over the 6-week period. However, within the first 2 weeks, the mice who ate during their normal sleeping phase weighed significantly more than the other mice. By the end of the study, the mice who ate when they should be sleeping had a 48% boost to their body weight, on average, compared to a 20% increase in the mice who ate the high-fat diet during their normal waking hours."
Many living organisms-from plants to fruit flies to humans-have internal biological clocks, or circadian rhythms, that govern our daily cycles of sleep and activity. These internal clocks are tied to cycles of light and darkness. Several recent studies have found that circadian clocks can affect metabolism in animals, suggesting that the timing of meals might influence whether incoming calories are burned or stored as fat.
To take a closer look, Dr Fred Turek, Deanna M. Arble and their colleagues at Northwestern University designed a study to search for a direct link between meal times and body weight. Their research is supported by NIH's National Institute on Aging (NIA) and National Heart, Lung and Blood Institute (NHLBI).
For 6 weeks, mice were fed a high-fat diet either during a 12-hour dark phase, when the mice are normally active, or during a 12-hour light phase, when the mice are normally resting. The mice could eat as much as they wanted during their assigned feeding periods, but the food was removed during the remaining 12 hours each day. The study was described in the 3 September 2009 advance online edition of Obesity.
The researchers found that both groups of mice had similar levels of activity and calorie consumption over the 6-week period. However, within the first 2 weeks, the mice who ate during their normal sleeping phase weighed significantly more than the other mice. By the end of the study, the mice who ate when they should be sleeping had a 48% boost to their body weight, on average, compared to a 20% increase in the mice who ate the high-fat diet during their normal waking hours."
Red Wine Chemical May One Day Treat Diabetes
The more common form of diabetes, Type 2, is a disease of fat people.
"Resveratrol, found in red wine, was found to lower blood sugar levels and improve insulin levels when injected directly into the brains of mice fed very high-calorie diets in a study conducted by researchers at the University of Texas Southwestern Medical Center (UTSW).
The finding suggests that the brain plays a key role in resveratrol’s beneficial effect on diabetes and that the benefits may occur independently of diet and body weight."
Friday, October 09, 2009
Albany Medical College enters agreement with Aegis
"Albany Medical College has entered into an agreement with Aegis Therapeutics LLC that could speed the development and commercialization of an anti-obesity peptide that could also benefit people with Type 2 diabetes.
The pact authorizes San Diego-based Aegis to develop a partnership with a pharmaceutical company, with the goal of beginning human clinical trials of the OB-3 peptide. The peptide was discovered by researchers at the Albany, N.Y., medical college.
If successful, the trials could result in the new drug becoming commercially available.
Dr. Patricia Grasso, associate professor of medicine at Albany Med, said the school’s researchers have developed a synthetic fragment of leptin, a protein hormone, that decreases appetite and increases metabolism. This has resulted in significant weight loss and lower blood glucose levels in the mice and rats.
'Now we hope to demonstrate that the OB-3 peptide can be similarly effective in humans,' she said."
The pact authorizes San Diego-based Aegis to develop a partnership with a pharmaceutical company, with the goal of beginning human clinical trials of the OB-3 peptide. The peptide was discovered by researchers at the Albany, N.Y., medical college.
If successful, the trials could result in the new drug becoming commercially available.
Dr. Patricia Grasso, associate professor of medicine at Albany Med, said the school’s researchers have developed a synthetic fragment of leptin, a protein hormone, that decreases appetite and increases metabolism. This has resulted in significant weight loss and lower blood glucose levels in the mice and rats.
'Now we hope to demonstrate that the OB-3 peptide can be similarly effective in humans,' she said."
Thursday, October 08, 2009
The Calorie-Restriction Experiment
"Going back more than a half century to an experiment at Cornell University in the mid-1930s, calorie restriction has been shown again and again to extend the lives of mice, rats and other animals."
Wednesday, October 07, 2009
Body's Circadian Rhythm Tightly Entwined With Blood Sugar Control
"Scientists have long struggled to understand the body's biological clock. Its tick-tock wakes us up, reminds us to eat and tells us when to go to bed. But what sets that circadian rhythm?
New research now shows that daily fluctuations in powerful hormones called glucocorticoids directly synchronize the biological clock as an integral part of our mechanism for regulating blood sugar.
'The most surprising part of our findings is that our internal biologic rhythms are embedded directly into another pathway, one that is essential to regulate metabolism,' said senior study author Brian Feldman, MD, PhD, assistant professor of pediatric endocrinology at the Stanford University School of Medicine. Feldman also practices at Lucile Packard Children's Hospital.
The new findings give the first in vivo evidence of a direct link between glucocorticoid hormones and genes that regulate our biological clock. The research may eventually help doctors reduce disabling side effects of glucocorticoid drugs such as prednisone, Feldman said. The work could also help diabetics control their blood sugar levels and may shed light on why night-shift workers are at risk for obesity and diabetes.
The study will be published online Oct. 5 in Proceedings of the National Academy of Sciences. Feldman worked previously at the University of California-San Francisco, where much of the research was conducted.
Feldman's team began their experiments by applying a synthetic glucocorticoid to dishes of mouse and human stem cells to see which genes responded. To the team's surprise, three genes known to control the biological clock changed their activity in a direct response to the hormone."
New research now shows that daily fluctuations in powerful hormones called glucocorticoids directly synchronize the biological clock as an integral part of our mechanism for regulating blood sugar.
'The most surprising part of our findings is that our internal biologic rhythms are embedded directly into another pathway, one that is essential to regulate metabolism,' said senior study author Brian Feldman, MD, PhD, assistant professor of pediatric endocrinology at the Stanford University School of Medicine. Feldman also practices at Lucile Packard Children's Hospital.
The new findings give the first in vivo evidence of a direct link between glucocorticoid hormones and genes that regulate our biological clock. The research may eventually help doctors reduce disabling side effects of glucocorticoid drugs such as prednisone, Feldman said. The work could also help diabetics control their blood sugar levels and may shed light on why night-shift workers are at risk for obesity and diabetes.
The study will be published online Oct. 5 in Proceedings of the National Academy of Sciences. Feldman worked previously at the University of California-San Francisco, where much of the research was conducted.
Feldman's team began their experiments by applying a synthetic glucocorticoid to dishes of mouse and human stem cells to see which genes responded. To the team's surprise, three genes known to control the biological clock changed their activity in a direct response to the hormone."
Polyphenol found in turmeric reduces weight gain in animal studies
"According to a Tufts University, Boston, MA study funded by a grant from the United States Department of Agriculture and released to the media on May 18, 2009, curcumin, the major polyphenol found in turmeric, appears to reduce weight gain in mice and suppress the growth of fat tissue in mice and cell models. Can it also stop humans from gaining weight?"
Gene transfer can help ailing heart heal itself
"[C]oronary artery disease, hypertension or high blood pressure, and diabetes" are all related to overweight/obesity.
"In a major breakthrough, scientists jump-started a failing heart by transferring a gene, which could help the heart heal itself.I know that rabbits are not rodents.
The breakthrough also offers a tantalizing glimpse of a day when “closed heart surgery” via gene therapy is as commonly prescribed as today’s cocktail of drugs.
Five million people in the US have heart failure, about 550,000 new cases are diagnosed each year, and more than 287,000 people die each year of heart failure, according to the US Center for Disease Control and Prevention.
The most common causes of heart failure are coronary artery disease, hypertension or high blood pressure, and diabetes.
Heart failure is a condition where the heart cannot pump enough blood and oxygen to meet the needs of other body organs.
'We hope that our study will lead some day to the development of new genetic-based therapies for heart failure patients,' said Todd J. Herron, study co-author and professor at the University of Michigan (U-M).
Herron and colleagues treated heart muscle cells from the failing hearts of rabbits and humans with a virus modified to carry a gene which produces a protein that enables heart cells to contract normally."
"...Rodentia does not include rabbits; rabbits differ from rodents in having an extra pair of incisors and in other skeletal features."Close enough.
Whatever it takes to help the overfat.
Tuesday, October 06, 2009
In Mouse Model Scientists Find Obesity Alone Does Not Cause Arthritis
"The link between obesity and osteoarthritis may be more than just the wear and tear on the skeleton caused by added weight.
A Duke University study has found that the absence of the appetite hormone leptin can determine whether obese mice experience arthritis, no matter how heavy they are.
'We were completely surprised to find that mice that became extremely obese had no arthritis if their bodies didn't have leptin,' said Farshid Guilak, Ph.D., director of orthopaedic research in the Duke Department of Surgery. 'Although there was some earlier evidence that leptin might be involved in the arthritis disease process, we didn't think that there would be no arthritis at all.'"
A Duke University study has found that the absence of the appetite hormone leptin can determine whether obese mice experience arthritis, no matter how heavy they are.
'We were completely surprised to find that mice that became extremely obese had no arthritis if their bodies didn't have leptin,' said Farshid Guilak, Ph.D., director of orthopaedic research in the Duke Department of Surgery. 'Although there was some earlier evidence that leptin might be involved in the arthritis disease process, we didn't think that there would be no arthritis at all.'"
Study offers clues on diet benefits without the diet
"Experiments which mimicked a low-calorie diet by tinkering with genes in mice extended their lives and prevented disease, and a drug that has the same effect could give people longer, healthier lives, scientists said on Thursday...
Deleting S6K1 meant the mice's bodies behaved in a similar way to mammals whose calorie intake is restricted, they said.
'These mice were resistant to type 2 diabetes... and they also appeared to have reduced incidence of the mouse-equivalent of osteoporosis -- so they had stronger bones,' Withers said.
Balance, strength and coordination all improved in the knockout mice, and they were more inquisitive, suggesting their brains were healthier...
Most calorie restriction studies have found that a lifetime of deprivation is needed to achieve the longer-life benefits, and many researchers are working on ways to replicate the findings with drugs."
Deleting S6K1 meant the mice's bodies behaved in a similar way to mammals whose calorie intake is restricted, they said.
'These mice were resistant to type 2 diabetes... and they also appeared to have reduced incidence of the mouse-equivalent of osteoporosis -- so they had stronger bones,' Withers said.
Balance, strength and coordination all improved in the knockout mice, and they were more inquisitive, suggesting their brains were healthier...
Most calorie restriction studies have found that a lifetime of deprivation is needed to achieve the longer-life benefits, and many researchers are working on ways to replicate the findings with drugs."
Discovery Of Gene That Protects High-Fat-Diet Mice From Obesity
"University of Michigan researchers have identified a gene that acts as a master switch to control obesity in mice. When the switch is turned off, even high-fat-diet mice remain thin.
Deleting the gene, called IKKE, also appears to protect mice against conditions that, in humans, lead to Type 2 diabetes, which is associated with obesity and is on the rise among Americans, including children and adolescents."
Deleting the gene, called IKKE, also appears to protect mice against conditions that, in humans, lead to Type 2 diabetes, which is associated with obesity and is on the rise among Americans, including children and adolescents."
Leptin-Serotonin Pathway Offers New Clues For Obesity And Osteoporosis Prevention
"New research from Columbia University Medical Center has illuminated a previously unknown leptin-serotonin pathway in the brain that simultaneously promotes appetite and bone mass accrual. The research, which explains how leptin - well-known appetite-suppressing hormone - acts in the brain, is published in the Sept. 4 issue of Cell.
When the leptin-serotonin pathway is turned on in mice, the researchers found, appetite increases, the animals eat more, gain weight, and their bone mass increases. When the pathway is turned off, mice eat less, lose weight, and their bones weaken. Furthermore, leptin was found to not act in the hypothalamus as previously thought, but in the brain stem acting on serotonin, a hormone that in the brain acts to control appetite, mood and anger."
When the leptin-serotonin pathway is turned on in mice, the researchers found, appetite increases, the animals eat more, gain weight, and their bone mass increases. When the pathway is turned off, mice eat less, lose weight, and their bones weaken. Furthermore, leptin was found to not act in the hypothalamus as previously thought, but in the brain stem acting on serotonin, a hormone that in the brain acts to control appetite, mood and anger."
Caloric Restriction Only Benefits Obese Mice: The Journal Of Nutrition
"If you are a mouse on the chubby side, then eating less may help you live longer.
For lean mice - and possibly for lean humans, the authors of a new study predict - the anti-aging strategy known as caloric restriction may be a pointless, frustrating and even dangerous exercise...
He and Michael Forster, of the University of North Texas Health Science Center, compared the life span and caloric intake of two genetically engineered strains of mice.
The 'fat' strain, known as C57BL/6, roughly doubles in weight over its adult life. That strain benefited from caloric restriction, Sohal said.
The 'lean' strain, DBA/2, does not become obese. Caloric restriction did not extend the life of these mice, confirming previous work by Forster and Sohal...
By measuring the animals' metabolic rate, Sohal and his colleagues came to a deceptively simple conclusion: Caloric restriction is only useful when, as in the case of the obese mice, an animal eats more than it can burn off.
'Your energy expenditure and your energy intake should be in balance,' Sohal said.
'It's as simple as that. And how do you know that? By gain or loss of weight. (sic)
'The whole thing is very commonsensical.'
For humans of normal weight, Sohal strongly cautions against caloric restriction. In a 2003 study, he and Forster found that caloric restriction begun in older mice - both in DBA and leaner C57 individuals - actually shortened life span...
Sohal's study is not the first to question the allegedly universal benefits of caloric restriction. A study by Ross et al. published in Nature in 1976 ('Dietary practices and growth responses as predictors of longevity') found that caloric restriction works best in mice that gain weight rapidly in early adulthood, Sohal said."
For lean mice - and possibly for lean humans, the authors of a new study predict - the anti-aging strategy known as caloric restriction may be a pointless, frustrating and even dangerous exercise...
He and Michael Forster, of the University of North Texas Health Science Center, compared the life span and caloric intake of two genetically engineered strains of mice.
The 'fat' strain, known as C57BL/6, roughly doubles in weight over its adult life. That strain benefited from caloric restriction, Sohal said.
The 'lean' strain, DBA/2, does not become obese. Caloric restriction did not extend the life of these mice, confirming previous work by Forster and Sohal...
By measuring the animals' metabolic rate, Sohal and his colleagues came to a deceptively simple conclusion: Caloric restriction is only useful when, as in the case of the obese mice, an animal eats more than it can burn off.
'Your energy expenditure and your energy intake should be in balance,' Sohal said.
'It's as simple as that. And how do you know that? By gain or loss of weight. (sic)
'The whole thing is very commonsensical.'
For humans of normal weight, Sohal strongly cautions against caloric restriction. In a 2003 study, he and Forster found that caloric restriction begun in older mice - both in DBA and leaner C57 individuals - actually shortened life span...
Sohal's study is not the first to question the allegedly universal benefits of caloric restriction. A study by Ross et al. published in Nature in 1976 ('Dietary practices and growth responses as predictors of longevity') found that caloric restriction works best in mice that gain weight rapidly in early adulthood, Sohal said."
Subscribe to:
Posts (Atom)