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Sympathetic stimulation of glucose uptake in insulin-sensitive tissues
Prof Tore Bengtsson
Physiology (Wenner-Gren Institute)
Swedish Research Council - Vetenskapsrådet (VR)
Obesity is a major inducer of type 2 diabetes and more than 150 million people worldwide suffer from type 2 diabetes. Stress has been proposed as one potential contributor to Type II diabetes but there are surprisingly few studies on this topic. Most attempts to treat type 2 diabetes have focused on improving insulin signaling. However, lately, great interest has developed in identifying insulin-independent mechanisms in order to find new treatments. We have found compelling evidence that activation of adrenergic receptors lead to an insulin-independent mechanism that increases glucose uptake in skeletal muscle. We have found that stimulation of beta2-AR in muscle, in addition to increasing cAMP levels, also activates PI3K (an important kinase normally associated with insulin-signaling) via an unknown mechanism. The beta-adrenergic activation of PI3K in skeletal muscle cells leads to an increase in glucose uptake of the same magnitude as the one mediated by insulin (but probably not through the same glucose transporters). In this application we want to investigate the signaling proteins and mechanisms of action used by adrenergic receptors to activate glucose uptake in muscle cells. It is of considerable importance to understand how adrenergic signaling leads to glucose uptake and the interplay between the insulin and adrenergic pathways. This can have great impact on our understanding and development of potential new treatments of type 2 diabetes.
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