Co-chaired by Jürgen Wess, NIDDK and Derek LeRoith, NIDDK

Conference Room E1/E2, Natcher Conference Center

The growing epidemic of obesity-associated type 2 diabetes represents one of the major threats to human health in the 21st century. To gain insight into the pathophysiology of type 2 diabetes and to develop new treatment protocols, it is essential to characterize the molecular components and signaling networks critical for beta-cell function and glucose and energy homeostasis. During the past few years, NIH researchers have used gene targeting and transgenic techniques to develop novel mouse models to study the molecular basis of type 2 diabetes and glucose and energy homeostasis. Phenotypical analysis of these mutant animals has led to a wealth of novel findings, including the identification of receptors, G proteins, and other signaling molecules that play key roles in these processes. Given the preeminent importance of this topic, this mini-symposium should be timely and of great interest for a wide audience.

Program:

A Mouse Model of Type 2 Diabetes: Pathophysiology and Therapeutic Implications
Derek LeRoith, NIDDK

Role of M3 Muscarinic Acetylcholine Receptors in the Regulation of Body Weight, Beta-cell Function, and Glucose Homeostasis
Jürgen Wess, NIDDK

Role of the Gnas Locus in the Regulation of Energy and Glucose Metabolism
Lee S. Weinstein, NIDDK

Cytokine-mediated Stat5 Signaling Is Required for Insulin Secretion and Glucose Homeostasis
Lothar Hennighausen, NIDDK

Role of Cyclic Nucleotide Phosphodiesterase 3B (PDE3B) in Regulation of Energy Homeostasis
Vincent C. Manganiello, NHLBI

The Hexosamine Signaling Pathway and Diabetes Mellitus
John A. Hanover, NIDDK