Suppr超能文献

[非胰岛素依赖型糖尿病中胰岛素分泌受损的发病机制]

[Pathogenesis of impaired insulin secretion in NIDDM].

作者信息

Yamada Y, Seino Y

机构信息

Department of Metabolism and Clinical Nutrition, Kyoto University Graduate School of Medicine.

出版信息

Nihon Rinsho. 1999 Mar;57(3):534-8.

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.

摘要

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。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验