Why is it that men and women put on those extra kilos in different areas of the body? The answer may not be far away as researchers are close to revealing vital sex differences in men and women concerning fat storage.
The research has indicated that fat is genetically different in men and women.
"Given the difference in gene expression profiles, a female fat tissue won't behave anything like a male fat tissue and vice versa," said Deborah Clegg, of the UT Southwestern Medical Center.
"The notion that fat cells between males and females are alike is inconsistent with our findings," he said.
Mice store their fat similar to humans in a sexually dimorphic pattern. Just like human males, male mice store their fat in the belly and midsection area while females store fat in their hips, thighs and buttocks...
Monday, August 30, 2010
Exercise 'can control appetite'
Exercise not only burns off calories, it can reduce feelings of hunger, scientists have said.
The findings suggest a "double whammy" benefit that may help the overweight to slim.
Researchers studying obese mice found that exercise restored the sensitivity of brain cells involved in controlling appetite.
The change increased satiety - or "feeling full" - in the animals and led to a reduction in food intake...
The findings suggest a "double whammy" benefit that may help the overweight to slim.
Researchers studying obese mice found that exercise restored the sensitivity of brain cells involved in controlling appetite.
The change increased satiety - or "feeling full" - in the animals and led to a reduction in food intake...
Saturday, August 21, 2010
Novel Diabetes Hope Comes from Chinese Herbs
Emodin, a natural product that can be extracted from various Chinese herbs including Rheum palmatum and Polygonum cuspidatum, shows promise as an agent that could reduce the impact of type 2 diabetes. Findings published in this month's edition of the British Journal of Pharmacology show that giving emodin to mice with diet-induced obesity lowered blood glucose and serum insulin, improved insulin resistance and lead to more healthy levels of lipid in the blood. It also decreased body weight and reduced central fat mass..
Thursday, August 12, 2010
Wouldn’t it be Great if You Could Pop a Pill and Lose Weight?
And wouldn't it be great if that pill weren't something advertised on late-night TV, but rather a legitimate treatment? A drug called rimonabant, introduced in Europe, seemed to fit the bill at first, but it was pulled from the market in late 2008 due to concerns about psychiatric side effects.
The story doesn't end there, though. New research on animals suggests that a second generation of drugs may treat obesity without those side effects. A presentation at the International Congress on Obesity in Stockholm, Sweden, revealed a treatment that has the same weight-loss effect as rimonabant, but without impacting the brain.
What's different? The new drug, currently called TM38837, does not affect peripheral organs and tissues. Rimonabant, however, didn't discriminate. According to earlier research, rimonabant doubled the risk of disorders such as depression and suicide.
In their new work, scientists tried the second-generation drug on mice and rats. After a five-week course of treatment, the mice had lost 22 to 26 percent more weight than mice in a control group. The rats had lost 14 percent more than the controls. In both cases, weight loss from TM38837 was the same as weight loss from rimonabant. Separate studies, including dissections and behavioral tests, showed that the drug was less likely to impact the brains of test animals...
The story doesn't end there, though. New research on animals suggests that a second generation of drugs may treat obesity without those side effects. A presentation at the International Congress on Obesity in Stockholm, Sweden, revealed a treatment that has the same weight-loss effect as rimonabant, but without impacting the brain.
What's different? The new drug, currently called TM38837, does not affect peripheral organs and tissues. Rimonabant, however, didn't discriminate. According to earlier research, rimonabant doubled the risk of disorders such as depression and suicide.
In their new work, scientists tried the second-generation drug on mice and rats. After a five-week course of treatment, the mice had lost 22 to 26 percent more weight than mice in a control group. The rats had lost 14 percent more than the controls. In both cases, weight loss from TM38837 was the same as weight loss from rimonabant. Separate studies, including dissections and behavioral tests, showed that the drug was less likely to impact the brains of test animals...
Sunday, August 08, 2010
Light Shed on Triglyceride Metabolism
New findings reported in the July issue of Cell Metabolism, are offering new leads as to why some people might suffer from high levels of triglycerides. High triglycerides are a risk factor for atherosclerosis and cardiovascular disease. They can also lead to inflammation of the pancreas, the researchers said...
It seems that a protein known as GPIHBP1 is the key. Mice lacking that protein end up with LPL built up outside of their muscle and fat tissue instead of where it belongs in capillaries. They show that GPIHBP1 normally sits on the surface of capillary cells, where it actively transports LPL.
The new findings offer an explanation for what had been a surprising finding; Gpihbp1-deficient mice develop severe hypertriglyceridemia, even when they eat a normal diet of mouse chow. Very recently, other researchers have also shown that some people with elevated triglyceride levels carry mutations in their GPIHBP1 gene...
It seems that a protein known as GPIHBP1 is the key. Mice lacking that protein end up with LPL built up outside of their muscle and fat tissue instead of where it belongs in capillaries. They show that GPIHBP1 normally sits on the surface of capillary cells, where it actively transports LPL.
The new findings offer an explanation for what had been a surprising finding; Gpihbp1-deficient mice develop severe hypertriglyceridemia, even when they eat a normal diet of mouse chow. Very recently, other researchers have also shown that some people with elevated triglyceride levels carry mutations in their GPIHBP1 gene...
Saturday, August 07, 2010
Calling all Obelixes! Hope at home - Indian researchers join global scramble to develop anti-obesity pill
New Delhi, July 31: A team of industry researchers in India has synthesised novel compounds that interfere with weight-gaining mechanisms in the body and joined an international scramble to develop a new class of anti-obesity pills.
The team at Dr Reddy’s Laboratories (DRL), Hyderabad, has shown in laboratory studies that one of these compounds, code-named 22g, helped gluttonous and obese mice lose 8 per cent of their body weight after seven days of oral medication...
The team at Dr Reddy’s Laboratories (DRL), Hyderabad, has shown in laboratory studies that one of these compounds, code-named 22g, helped gluttonous and obese mice lose 8 per cent of their body weight after seven days of oral medication...
ew loci for blood lipids identified; functional role of 1p13 locus detailed
Bethesda, MD and Boston, MA - Two new studies published this week provide further insights into the genetic underpinnings of variations in blood lipid levels [1,2]. In one large-scale genomewide association study (GWAS), researchers identified 95 loci that showed associations with blood lipid levels, while another group performed a detailed functional genomics analysis showing how a locus on chromosome 1p13, previously associated with low LDL-cholesterol levels and MI, regulates LDL-cholesterol levels.
"The two papers are highly complementary," Dr Sekar Kathiresan (Massachusetts General Hospital, Boston), a senior investigator of both studies, told heartwire. "The reason they're so complementary is that the first paper, the GWAS paper, puts down 95 stakes in the sand, while the second paper drills down on one of those stakes. We think the mapping effort, the GWAS paper, is incredibly important simply based on the scale of the effort. It's safe to say it's the largest genetics study done to date, and these 95 loci explain about 25% of the genetic component for lipid levels, which is among the largest proportion of variation evaluated to date."
The two studies are published in the August 5, 2010 issue of Nature...
To show that SORT1 is the causal gene, the researchers manipulated the gene in mice. With small interfering RNA "knockdown" and "viral overexpression" in the mouse liver, the researchers showed that the upregulation of SORT1 led to significantly lower LDL-cholesterol levels, as much as 80% lower, and that silencing SORT1 increased LDL cholesterol approximately 200%.
"Using these experiments in mice, we were able to prove that sortilin is the right gene for the LDL effect at the chromosome 1 locus," Kathiresan told heartwire. "And then, finally, if sortilin is the right gene, how does sortilin lower LDL cholesterol? We showed that the physiologic mechanism is that higher levels of sortilin lead to less secretion of very low-density lipoprotein (vLDL) from the liver, and vLDL is the precursor to LDL. Having less of the precursor around leads to less LDL, and this was the final piece of the puzzle."...
"The two papers are highly complementary," Dr Sekar Kathiresan (Massachusetts General Hospital, Boston), a senior investigator of both studies, told heartwire. "The reason they're so complementary is that the first paper, the GWAS paper, puts down 95 stakes in the sand, while the second paper drills down on one of those stakes. We think the mapping effort, the GWAS paper, is incredibly important simply based on the scale of the effort. It's safe to say it's the largest genetics study done to date, and these 95 loci explain about 25% of the genetic component for lipid levels, which is among the largest proportion of variation evaluated to date."
The two studies are published in the August 5, 2010 issue of Nature...
To show that SORT1 is the causal gene, the researchers manipulated the gene in mice. With small interfering RNA "knockdown" and "viral overexpression" in the mouse liver, the researchers showed that the upregulation of SORT1 led to significantly lower LDL-cholesterol levels, as much as 80% lower, and that silencing SORT1 increased LDL cholesterol approximately 200%.
"Using these experiments in mice, we were able to prove that sortilin is the right gene for the LDL effect at the chromosome 1 locus," Kathiresan told heartwire. "And then, finally, if sortilin is the right gene, how does sortilin lower LDL cholesterol? We showed that the physiologic mechanism is that higher levels of sortilin lead to less secretion of very low-density lipoprotein (vLDL) from the liver, and vLDL is the precursor to LDL. Having less of the precursor around leads to less LDL, and this was the final piece of the puzzle."...
All-Nighters May Increase Fat Levels in Blood
Disruptions to a person's normal sleep cycle, such as pulling several all-nighters, could lead to an increase in harmful triglycerides in the blood, a new study on mice suggests.
Though further studies are needed to firm up whether the same holds for humans, scientists often use these rodents as models for human systems.
The new findings could have implications for understanding the health effects of night shifts, 14-hour work days and transoceanic flights. High levels of triglycerides in the blood are a risk factor for heart disease and obesity – not only in mice, but also potentially in people, the researchers say...
Though further studies are needed to firm up whether the same holds for humans, scientists often use these rodents as models for human systems.
The new findings could have implications for understanding the health effects of night shifts, 14-hour work days and transoceanic flights. High levels of triglycerides in the blood are a risk factor for heart disease and obesity – not only in mice, but also potentially in people, the researchers say...
Insufficient ALA could be linked to obesity trend
A new study suggests that a deficiency in alpha-linoleic acid (omega-3) coupled with a chronic excess of linoleic acid (omega-6) could lead to ‘inherited obesity’.
The study, published in the Journal of Lipid Research, describes an increase in fat mass of mice over several generations when fed an ‘unbalanced Western diet’.
In addition to trans-generational weight gain, the research also observed the onset of metabolic disorders such as insulin resistance, and the expression of the inflammatory genes involved in obesity as generations advanced.
“Collectively, our data show that continuous exposure to a high-fat diet combined with a high LA:LNA [omega-6:omega-3] ratio over generations triggers a discrete and steady increase in inflammatory stimuli, accompanied by enhancement of fat mass” wrote the researchers.
Unbalanced Intake
The beneficial role that polyunsaturated fatty acids can have on health is well established. However when their intake is unbalanced, these essential fatty acids can enhance factors that can induce obesity, and may have serious long-term effects on human health.
During the last forty years Western societies have seen increases in the level of calories ingested, alongside an increase of over 250 percent in levels omega-6 intake and a fall in levels of omega-3 of 40 percent. This change in diet has coincided with a steady rise in obesity levels through the generations.
Over this time the ratio of omega-6 to omega-3 in a typical Western diet has shifted from the recommended 5-to-1, to 15-to-1 in much of Europe, and can be as high as 40-to-1 in the United States.
Alpha-linoleic acid (ALA) omega-3 is an essential fatty acid that the body cannot make, and therefore must be consumed in the diet. Good sources of ALA include: flaxseed, soybeans, walnuts, and olive oil. The U.S Institute of Medicine recommends an ALA intake of 1.6 grams per day for men and 1.1 grams per day for women.
Assessing the consequences
The new research, led by Gérard Ailhaud at the Université de Nice Sophia-Antipolis in France, exposed several generations of mice to a high omega-6 and low omega-3 "Western" diet and assessed the consequences.
The mice were given unrestricted access to food and water (ad libitum conditions) over several generations in order to allow the mice to self-regulate the intake according to biological needs.
“We chose purposely ad libitum conditions to expose both male and female mice across several generations to a Western-like diet” the researchers explain.
Trans-generational inheritance
The results of the study observe that under conditions of genetic stability and with no change to routine, four generations of a ‘Western-like fat diet’ were sufficient to gradually increase fat mass.
“A gradual trans-generational increase in adiposity can occur in mice fed a Western-like fat diet” wrote the researchers.
The study suggests that an unbalanced diet can lead to changes in the expression of genes that control growth and immune functions.
A gene expression analysis of fat tissue over several generations of the mice observed “discrete and steady changes in certain important players, such as colony stimulating factor-3 (CSF3) and Nocturnin.”
The researchers said “Our data show that expression of CSF-3 increased over generations in mice. These results strongly suggest a role for CSF-3 in stimulating growth of adipocyte progenitors.”...
The study, published in the Journal of Lipid Research, describes an increase in fat mass of mice over several generations when fed an ‘unbalanced Western diet’.
In addition to trans-generational weight gain, the research also observed the onset of metabolic disorders such as insulin resistance, and the expression of the inflammatory genes involved in obesity as generations advanced.
“Collectively, our data show that continuous exposure to a high-fat diet combined with a high LA:LNA [omega-6:omega-3] ratio over generations triggers a discrete and steady increase in inflammatory stimuli, accompanied by enhancement of fat mass” wrote the researchers.
Unbalanced Intake
The beneficial role that polyunsaturated fatty acids can have on health is well established. However when their intake is unbalanced, these essential fatty acids can enhance factors that can induce obesity, and may have serious long-term effects on human health.
During the last forty years Western societies have seen increases in the level of calories ingested, alongside an increase of over 250 percent in levels omega-6 intake and a fall in levels of omega-3 of 40 percent. This change in diet has coincided with a steady rise in obesity levels through the generations.
Over this time the ratio of omega-6 to omega-3 in a typical Western diet has shifted from the recommended 5-to-1, to 15-to-1 in much of Europe, and can be as high as 40-to-1 in the United States.
Alpha-linoleic acid (ALA) omega-3 is an essential fatty acid that the body cannot make, and therefore must be consumed in the diet. Good sources of ALA include: flaxseed, soybeans, walnuts, and olive oil. The U.S Institute of Medicine recommends an ALA intake of 1.6 grams per day for men and 1.1 grams per day for women.
Assessing the consequences
The new research, led by Gérard Ailhaud at the Université de Nice Sophia-Antipolis in France, exposed several generations of mice to a high omega-6 and low omega-3 "Western" diet and assessed the consequences.
The mice were given unrestricted access to food and water (ad libitum conditions) over several generations in order to allow the mice to self-regulate the intake according to biological needs.
“We chose purposely ad libitum conditions to expose both male and female mice across several generations to a Western-like diet” the researchers explain.
Trans-generational inheritance
The results of the study observe that under conditions of genetic stability and with no change to routine, four generations of a ‘Western-like fat diet’ were sufficient to gradually increase fat mass.
“A gradual trans-generational increase in adiposity can occur in mice fed a Western-like fat diet” wrote the researchers.
The study suggests that an unbalanced diet can lead to changes in the expression of genes that control growth and immune functions.
A gene expression analysis of fat tissue over several generations of the mice observed “discrete and steady changes in certain important players, such as colony stimulating factor-3 (CSF3) and Nocturnin.”
The researchers said “Our data show that expression of CSF-3 increased over generations in mice. These results strongly suggest a role for CSF-3 in stimulating growth of adipocyte progenitors.”...
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