[Pathogenesis of impaired insulin secretion in NIDDM]

Abstract

The most important role of pancreatic beta-cells is the insulin secretion responding to the plasma glucose level. Molecular biological and electrophysiological approaches have been revealing the molecular mechanism of glucose-stimulated insulin secretion. A lot of key molecules of the systems, including GLUT2, glucokinase, SUR1, Kir6.2 and CD38, have been cloned and characterized whether the mutations in these genes are responsible for the pathogenesis of non-insulin-dependent diabetes mellitus (NIDDM). In this paper, we summarized the recent advances concerning pathogenesis of NIDDM in respect of impaired insulin secretion from pancreatic beta-cells.