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."
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