Resveratrol is a potent antioxidant found in the skin of red grapes and red wine. Previous research suggests that resveratrol is associated with increased life span in obese older mice. Reduced mitochodrial function (the metabolic conversion of food to energy) and exercise capacity are linked with aging. Now research reports that resveratrol increased exercise expenditure and decreased the risk of insulin resistance and obesity in obese mice.
The study, published in the journal Cell, investigated the effects of resveratrol on mitochodrial function and aerobic capacity in mice. Researchers at the Institute of Genetics and Molecular and Cellular Biology in Illkirch, France added either 200 or 400 mg per kilogram resveratrol to a high fat diet or regular diet, for 15 weeks. Food intake, body fat and body weight measurements, endurance tests, and fasting insulin levels were obtained from the mice.
Researchers found that the mice who received the resveratrol gained less weight than the mice who did not receive the supplement. Furthermore, the mice who received the resveratrol high fat diet weighed about the same as the mice on the regular diet without resveratrol. The resveratrol-fed mice had a decrease in body fat, with smaller fat cells. Findings also revealed that the resveratrol-fed mice had greater energy expenditure and enhanced mitochondrial activity. In addition, the resveratrol-fed mice had significantly decreased fasting insulin levels, indicating improved insulin sensitivity.
The study authors suggest that resveratrol increases the activity of the Sirt1 gene, which is linked with increased life span. "Importantly, resveratrol treatment protected mice against diet-induced-obesity and insulin resistance," the study authors write. "These pharmacological effects of resveratrol combined with the association of three Sirt1 SNPs and energy homeostasis in Finnish subjects implicates SIRT1 as a key regulator of energy and metabolic homeostasis."
REFERENCES:
1. Lagouge M et al. Resveratrol Improves Mitochondrial Function and Protects against Metabolic Disease by Activating SIRT1 and PGC-1alpha. Cell 2006 Nov 15; [Epub ahead of print].
Posted by Elaine Gavalas on December 12, 2006 03:44 PM
