Unraveling sympathetic influences on type II diabetes: Effects of ß-adrenergic stimulation of glucose uptake in skeletal muscles

Type II diabetes affects more than 150 million people in the world and the number is raising rapidly. Most attempts to treat type 2 diabetes have focused on improving insulin signaling and at present there is no definitive treatment. However, lately, great interest has developed in identifying insulin-independent mechanisms in order to find new treatments.

Our research has focused on the sympathetic regulation of glucose uptake in skeletal muscle. We have found compelling evidence that activation of adrenergic receptors lead to an insulin-independent mechanism that increases glucose uptake in skeletal muscle cells. The beta-adrenergic activation in skeletal muscle cells leads to an increase in glucose uptake of the same magnitude as the one mediated by insulin.

This project will dissect the signaling pathways and mechanisms utilized by adrenergic receptors to increase glucose uptake in skeletal muscle and clarify if these mechanisms are altered in type II diabetes. Our aim is to understand if activation of the sympathetic nervous system is positive or negative for type II diabetes. The experiments will be performed first in mice and later in humans.

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.