Yamada Y, Seino Y
Department of Metabolism and Clinical Nutrition, Kyoto University Graduate School of Medicine.
Nihon Rinsho. 1999 Mar;57(3):534-8.
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.
胰腺β细胞的最重要作用是根据血糖水平分泌胰岛素。分子生物学和电生理学方法一直在揭示葡萄糖刺激的胰岛素分泌的分子机制。该系统的许多关键分子，包括GLUT2、葡萄糖激酶、SUR1、Kir6.2和CD38，已被克隆并鉴定，这些基因的突变是否与非胰岛素依赖型糖尿病（NIDDM）的发病机制有关。在本文中，我们总结了关于胰腺β细胞胰岛素分泌受损方面非胰岛素依赖型糖尿病发病机制的最新进展。
