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REVIEWS
Department of Medicine, Samuel Lunenfeld Research Institute, Mt. Sinai Hospital, Toronto, Ontario, Canada
Submitted 22 February 2008 ; accepted in final form 24 December 2008
ABSTRACT
Glucagon is secreted from the
-cells of the pancreatic islets and regulates glucose homeostasis through modulation of hepatic glucose production. As elevated glucagon levels contribute to the pathophysiology of hyperglycemia in subjects with type 2 diabetes, reduction of glucagon receptor gene (Gcgr) activity represents a potential target for the treatment of T2DM. Herein, we review current concepts of glucagon action in hepatic and extrahepatic tissues and evaluate the therapeutic potential, mechanisms of action, and safety of reducing Gcgr signaling for the treatment of T2DM.
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