GLP-1 receptor signaling:: effects on pancreatic β-cell proliferation and survival

被引：123
|
作者：
Buteau, J.
机构：
[1] Univ Laval, Dept Anat & Physiol, Ste Foy, PQ G1V 4G5, Canada
[2] Hop Laval, Ctr Rech, Ste Foy, PQ G1V 4G5, Canada
来源：
DIABETES & METABOLISM | 2008年 / 34卷
关键词：
incretins; glucagon-like peptide-1; dipeptidyl-peptidase IV; beta-cell mass; apoptosis;
D O I：
10.1016/S1262-3636(08)73398-6
中图分类号：
R5 [内科学];
学科分类号：
1002 ; 100201 ;
摘要：
Type 2 diabetes is a metabolic disorder characterized by insulin resistance as well as a progressive deterioration of pancreatic beta-cell mass and function. Glucagon-like peptide 1 (GLP-1), an incretin hormone secreted by intestinal L cells, is a promising therapeutic agent in the treatment of diabetes. GLP-1 analogs and enhancers constitute a novel class of anti-diabetes medications which address both the insulin secretion defect as well as the decline in beta-cell mass. GLP-1 improves glucose-stimulated insulin secretion, restores glucose competence in glucose-resistant beta-cells, and stimulates insulin gene expression and biosynthesis. Furthermore, GLP-1 acts as a growth factor by promoting beta-cell proliferation, survival and neogenesis. This review focuses on the molecular mechanisms by which GLP-1 signaling induces beta-cell mass expansion. (C) 2008 Elsevier Masson SAS. All rights reserved.
引用
收藏
页码：S73 / S77
页数：5
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