ABSTRACT
Correspondence: Dr. Brian A.Hemmings, Friedrich Miescher-Institut, Maulbeerstrasse 66, CH-4058 Basel, Switzerland. Tel. +41 61 697 40 46; Fax +41 61 697 39 76; e-mail: hemmings@fmi.ch
INTRODUCTION
Diabetes mellitus is the most common metabolic disorder in humans. In only 5-10% of cases the illness is insulin-dependent and attributable to autoimmune destruction of insulin-secreting pancreatic β cells. The vast majority of patients fall into the category of noninsulin-dependent diabetes mellitus (NIDDM) or type 2 diabetes (reviewed in Kahn, 1998). In most cases NIDDM is of polygenic origin with a contribution of environmental factors, such as diet, age and physical activity (reviewed in Kahn et al., 1996). The disease is characterized by insulin resistance coupled with the failure of pancreatic β cells to compensate (Kahn et al., 1996). For this reason, considerable attention has been focused on the delineation of the insulin signaling pathway.
