The number of individuals with type 2 diabetes is reaching epidemic proportions. One of the main risk factors for developing type 2 diabetes is resistance of cells in the body (particularly liver, fat, and skeletal muscle cells) to the effects of the hormone insulin. Substantially reducing caloric intake enhances the sensitivity of skeletal muscle to insulin. Defining the molecular signals within skeletal muscle linking caloric restriction to improved insulin action could provide new targets for therapeutics to reduce insulin resistance and thereby lower an individual's risk of developing type 2 diabetes. In this context, a team of researchers led by Jerrold Olefsky, at the University of California at San Diego, La Jolla, has now found that the mouse protein Sirt1 has an integral role within skeletal muscle in linking caloric restriction to improved insulin action. Furthermore, they have identified the downstream molecular mechanism by which Sirt1 translates decreases in nutrient intake into enhanced skeletal muscle insulin sensitivity.
|Contact: Karen Honey|
Journal of Clinical Investigation