Two insulin related signalling pathways that are active in fat cells and control diet-induced obesity are reported in a paper published in Nature Communications this week. This new function of the insulin and insulin-like growth factor-1 (IGF-1) pathways in fat cells complements their known role in regulating the response to nutrients in many tissues.
Insulin and IGF-1 regulate cell division and differentiation of fat cells by binding to specific receptors on the cell surface. As some of their physiological effects overlap, the two pathways can compensate for each other in situations when one is defective, such as in many animal models used to study their function. Ronald Kahn and colleagues created mice that lack insulin and IGF-1 receptors specifically on fat cells. They found that these mice were much leaner than normal mice, did not develop symptoms of diabetes with age and, when fed a high-fat diet, did not put on any weight. The mice also burned more calories than normal mice at rest, although the precise reasons for this remained unclear.
The findings highlight the important role of insulin and IGF-1 signalling pathways in controlling fat tissue development and function as well as energy expenditure.