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

Diabetes Metab. 2008 Feb;34 Suppl 2:S73-7. doi: 10.1016/S1262-3636(08)73398-6.

Abstract

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.

Publication types

  • Review

MeSH terms

  • Cell Division
  • Cell Survival
  • Diabetes Mellitus, Type 2 / drug therapy*
  • Diabetes Mellitus, Type 2 / physiopathology
  • Dipeptidyl Peptidase 4
  • Dipeptidyl-Peptidase IV Inhibitors
  • Glucagon-Like Peptide-1 Receptor
  • Humans
  • Insulin-Secreting Cells / cytology*
  • Insulin-Secreting Cells / drug effects
  • Protease Inhibitors / therapeutic use
  • Receptors, Glucagon / physiology*
  • Signal Transduction

Substances

  • Dipeptidyl-Peptidase IV Inhibitors
  • GLP1R protein, human
  • Glucagon-Like Peptide-1 Receptor
  • Protease Inhibitors
  • Receptors, Glucagon
  • DPP4 protein, human
  • Dipeptidyl Peptidase 4