Diabetes News

Archive - 09 - 2012

Scientists Find Molecular Link to Obesity/Insulin Resistance in Mice

Posted by dlife on Fri, Sep 28, 12, 10:18 AM 0 Comment

September 25, 2012 (Newswise) Flipping a newly discovered molecular switch in white fat cells enabled mice to eat a high-calorie diet without becoming obese or developing the inflammation that causes insulin resistance, report scientists from Dana-Farber Cancer Institute.The researchers say the results, to be published in the Sept. 28 issue of the journal Cell, provide the first known molecular link between thermogenesis (burning calories to produce heat) and the development of inflammation in fat cells.These two processes had been previously thought to be controlled separately. Thermogenesis plays an important role in metabolism and maintaining healthy weight. Inflammation triggers insulin resistance, a precursor of diabetes.The researchers, led by Bruce Spiegelman, PhD, found that the protein TRPV4, a switch molecule, is highly expressed in white fat cells, which store excess calories and become engorged in obese individuals.For this study, the investigators bred mice lacking TRPV4 or administered a drug to deactivate it. In the absence of TRPV4, white cells turned on a set of genes that consume energy to produce heat, rather than storing the energy as excess fat. This "thermogenic" process normally occurs in brown or beige fat (commonly called "good fat"), which is found mostly in small animals and human infants to protect against cold.When the TRPV4-deficient mice were put on a high-calorie diet for several weeks, they did not become obese, and their level of fat cell inflammation and insulin resistance was lowered."We have identified a target that, when inhibited, can activate beige adipose tissue and suppress inflammation," said Spiegelman. "This role of TRPV4 as a mediator for both the thermogenic and pro-inflammatory programs in adipocytes, or fat cells, could offer an attractive target for treating obesity and related metabolic diseases."A co-activator protein, PGC-1 alpha, previously discovered in the Spiegelman laboratory, helps turn on thermogenesis to produce heat. In the new experiments, Spiegelman and his colleagues demonstrated that TRPV4 blocks PGC-1 alpha in white fat cells. Inhibiting TRPV4 in the experimental mice raised the expression of PGC-1 alpha and sparked thermogenesis.An experimental compound, GSK205, was used to inhibit TRPV4 in the animal studies. Spiegelman said that this technology has been licensed for further development to Ember Therapeutics, a company he co-founded. Spiegelman is an Ember consultant and shareholder.In terms of potential therapies, Spiegelman said that "any single new approach to something as complicated as metabolic disease is unlikely to work, but our experiments with TRPV4 showed the effectiveness of this strategy and it appears to be quite safe."The first author of the report is Li Ye, PhD, in the Spiegelman lab. Other authors are from Dana-Farber, Boston Childrens Hospital, The Scripps Research Institute, Jupiter, Fla., Duke University Medical Center, Durham, N.C., and Massachusetts General Hospital.The research was supported in part by National Institutes of Health grants (DK031405 and DK080261).Dana-Farber Cancer Institute ( is a principal teaching affiliate of the Harvard Medical School and is among the leading cancer research and care centers in the United States. It is a founding member of the Dana-Farber/Harvard Cancer Center (DF/HCC), designated a comprehensive cancer center by the National Cancer Institute. It provides adult care with Brigham and Women's Hospital as Dana-Farber/Brigham and Women's Cancer Center, and it provides pediatric care with Boston Children's Hospital as Dana-Farber/Children's Hospital Cancer Center. Dana-Farber is the top-ranked cancer center in New England, according to U.S. News & World Report, and one of the largest recipients among independent hospitals of National Cancer Institute and National Institutes of Health grant funding. Follow Dana-Farber on Twitter: @dana-farber or Facebook:

New Study Shows Family Health History Does Not Impact Consumer Knowledge of High-Sodium Diet Risks

Posted by dlife on Fri, Sep 28, 12, 09:48 AM 0 Comment

September 28, 2012 (Institute of Food Technology) Results from a new study in the Journal of Food Science, published by the Institute of Food Technologists (IFT), indicate that people with a family history of sodium-related diseases did not have more knowledge on the relationship between sodium consumption and risk of getting certain diseases than those with no history.Researchers from North Carolina State University analyzed data collected from 489 consumers who participated in a quantitative Internet survey designed to gather knowledge and attitudes towards dietary sodium, sodium in foods, and health. The consumers were divided into two groups: group one, for those who had no family history, and group two, for those that did. Results showed that having a disease history did not increase the level of knowledge that excess sodium intake increases the risk of getting diseases.While respondents overall were familiar with the concept a diet high in sodium intake could lead to increased risk of high blood pressure and stroke, only 10 percent of consumers indicated excess sodium as a possible cause of heart disease. Knowledge of bone disease risk was also poor; only 37 percent were aware that a diet high in sodium could negatively impact bone health. In contrast, 68 percent of respondents were able to link sodium intake and kidney disease.Additional survey findings showed most consumers were able to consistently identify that foods with high sodium were the same as foods with high salt.About IFT
For more than 70 years, IFT has existed to advance the science of food. Our nonprofit scientific societymore than 18,000 members from more than 100 countriesbrings together food scientists, technologists and related professions from academia, government, and industry. For more information, please visit

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