Researchers are increasingly becoming aware of the influence that fatacting as an endocrine organhas over other tissues in the body. A new report today in Nature is no exception. Barbara Kahn and her colleagues from Beth Israel Deaconess Medical Center in Boston have discovered that low levels of a certain protein in fat cellsa decrease that is, in fact, seen in people with type 2 diabetescan lead to insulin resistance in muscle and liver cells as well. "This paper clearly shows that fat also is important for whole-body insulin action," Kahn says. "We think fat releases a molecule that circulates to muscle and liver and impairs insulin signaling in those cells."

The hormone insulin normally instructs cells in your body to absorb glucose from the blood after a meal. It does so by prompting muscle and fat cells to dispatch glucose transporters to their membranes. But when cells do not respond to insulinas is the case in diabetesexcess glucose builds up in the blood. In this latest study, the researchers created mice lacking the main glucose transporter, GLUT4, only in fat cells. What they soon discovered, however, was that muscle and liver cells in these animals also stopped heeding insulin's call. "We're not saying that decreased GLUT4 in fat is the only cause of insulin resistance," Kahn notes, "but it is an important risk factor." And that knowledge, they hope, will lead them to new targets for therapy.