Biosingularity

Archive for the ‘metabolism’ Category

Eating more n-3 polyunsaturated fatty acids, commonly known as omega-3 fatty acids, may help carriers of a genetic variant on the perilipin 4 (PLIN4) gene locus lose weight more efficiently.

Led by Jose M. Ordovas, PhD, director of the Nutrition and Genomics Laboratory at the USDA HNRCA, researchers genotyped seven single nucleotide polymorphisms (SNPs), also known as gene variants, from men and women of mostly white European ancestry enrolled in the Genetics of Lipid Lowering Drugs and Diet Network (GOLDN) study and the Framingham Offspring Study. Carriers of the gene variant tended to weigh more and exhibit higher body mass index (BMI), which would increase their risk of becoming obese. Yet carriers with higher omega-3 fatty acid intakes tended to weigh less than carriers who consumed little or no omega-3 fatty acids. Read the rest of this entry »

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The machinery responsible for energy production in fat cells is working poorly as a result of obesity. Finnish research done at the University of Helsinki and the National Public Health Institute shows that this may aggravate and work to maintain the obese state in humans.

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Researchers at UT Southwestern Medical Center have found that a single gene might control whether or not individuals tend to pile on fat, a discovery that may point to new ways to fight obesity and diabetes.

“From worms to mammals, this gene controls fat formation,” said Dr. Jonathan Graff, associate professor of developmental biology and internal medicine at UT Southwestern and senior author of a study appearing in the Sept. 5 issue of Cell Metabolism. “It could explain why so many people struggle to lose weight and suggests an entirely new direction for developing medical treatments that address the current epidemic of diabetes and obesity.

“People who want to fit in their jeans might someday be able to overcome their genes.”
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A new Joslin Diabetes Center-led study has identified a protein found in fat cells that may play a major role in how fat is produced and stored, offering a new target for treatments to prevent obesity and reduce the risk for type 2 diabetes. This latest research appears in the August 2007 issue of Cell Metabolism.

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Abdominal fat, the spare tire that many of us carry, has long been implicated as a primary suspect in causing the metabolic syndrome, a cluster of conditions that includes the most dangerous heart attack risk factors: prediabetes, diabetes, high blood pressure, and changes in cholesterol.

But with the help of powerful new imaging technologies, a team of Howard Hughes Medical Institute (HHMI) researchers at Yale University School of Medicine has found that insulin resistance in skeletal muscle leads to alterations in energy storage that set the stage for the metabolic syndrome.

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Coffee is among the most widely consumed beverages in the world, and that the preponderance of scientific evidence suggests that moderate coffee consumption (3-5 cups per day) may be associated with reduced risk of certain disease conditions, such as Parkinson’s disease. Some research in neuropharamacology suggests that one cup of coffee can halve the risk of Parkinson’s disease. Other studies have found it reduces the risk of Alzheimer’s disease, kidney stones, gallstones, depression and even suicide.
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By giving ordinary adult mice a drug – a synthetic designed to mimic fat – Salk Institute scientist Dr. Ronald M. Evans is now able to chemically switch on PPAR-d, the master regulator that controls the ability of cells to burn fat. Even when the mice are not active, turning on the chemical switch activates the same fat-burning process that occurs during exercise. The resulting shift in energy balance (calories in, calories burned) makes the mice resistant to weight gain on a high fat diet.
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A relative of the anti-aging gene Klotho helps activate a hormone that can lower blood glucose levels in fat cells of mice, making it a novel target for developing drugs to treat human obesity and diabetes, UT Southwestern Medical Center researchers have found.

Dr. Makoto Kuro-o, associate professor of pathology, has reported that a relative of the anti-aging gene Klotho helps activate a hormone that can lower blood glucose levels in fat cells of mice. This discovery of a particular type of Klotho protein could eventually make it a novel target for developing drugs to treat human obesity and diabetes.
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Researchers at the University of California, San Diego, have constructed the first complete computer model of human metabolism. Available free on the Web, the model is a major step forward in the fledging field of systems biology, and it will help researchers uncover new drug pathways and understand the molecular basis of cancer and other diseases.

Read rest of this story on Technology Review site.

Caloric Restriction in non-obese people translates into less oxidative damage in muscle cells, according to a new study by scientists at Pennington Biomedical Research Center. As oxidative damage has been linked to aging, this could explain how limiting calorie intake without malnutrition extends life span.

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Civitarese and colleagues found that indeed fewer calories can improve whole body metabolism in conjunction with an increase in SIRT1 gene expression in skeletal muscle. These results raise the possibility that SIRT1 may contribute to more efficient metabolism, less oxidative stress, and increase longevity in humans as it does in lower organism. (Credit: Image courtesy of Public Library of Science)
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Researchers at the Institute of Genetics and Molecular and Cellular Biology in Illkirch, France have found that resveratrol boosts the exercise capacity of muscles in mice and protects against diet-induced insulin resistance and obesity. The research was published online on November 16, 2006 in the journal Cell.
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“Our study shows it is possible to increase lifespan in mice by modest but prolonged lowering of core body temperature,” said Bruno Conti, an associate professor at Scripps Research who led the study. “This longer lifespan was attained independent of calorie restriction.”
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Researchers at Harvard Medical School and Massachusetts General Hospital have identified how a molecular switch regulates fat and cholesterol production, a step that may help advance treatments for metabolic syndrome, the constellation of diseases that includes high cholesterol, obesity, type II diabetes, and high blood pressure. The study is now published in the online version of the scientific journal Nature and will appear in the August 10th print edition.
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Twelve years ago, scientists discovered leptin–the now-famous hormone that controls appetite, burns calories and performs other crucial physiological activities as well. But the precise mechanism(s) by which leptin carries out these metabolic tasks is still controversial. Now, researchers at the Albert Einstein College of Medicine of Yeshiva University have shown how leptin exerts some of its most important effects.

Their findings, reported in the July 5 issue of Cell Metabolism, suggest a novel approach for duplicating leptin’s actions when the body no longer responds to the hormone.
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