Insulin feedback action on pancreatic β-cell function

被引：90

作者：

Leibiger, IB ^{[1
]}

Leibiger, B ^{[1
]}

Berggren, PO ^{[1
]}

机构：

[1] Karolinska Inst, Karolinska Hosp, Dept Mol Med, Rolf Luft Ctr Diabet Res, S-17176 Stockholm, Sweden

来源：

FEBS LETTERS | 2002年 / 532卷 / 1-2期

关键词：

insulin; insulin receptor; insulin secretion; gene expression; diabetes mellitus;

D O I：

10.1016/S0014-5793(02)03627-X

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Pancreatic beta-cell function is essential for the regulation of glucose homeostasis and its impairment leads to diabetes mellitus. Besides glucose, the major nutrient factor, inputs from neural and Immoral components and intraislet cell-cell communication act together to guarantee an appropriate pancreatic beta-cell function. Data obtained over the last 5 years in several laboratories have revitalized a controversial concept, namely the autocrine feedback action of secreted insulin on beta-cell function. While, historically, insulin was suggested to exert a negative effect on beta-cells, recent data provide evidence for a positive role of insulin in transcription, translation, ion flux, insulin secretion and beta-cell survival. (C) 2002 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved.

引用

页码：1 / 6

页数：6

共 58 条

[1] Stimulation of acetyl-CoA carboxylase gene expression by glucose requires insulin release and sterol regulatory element binding protein 1c in pancreatic MIN6 β-cells [J].