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GLP-1 receptor signaling: effects on pancreatic beta-cell proliferation and survival Buteau JDiabetes Metab 2008[Feb]; 34 Suppl 2 (ä): S73-7Type 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.|Cell Division[MESH]|Cell Survival[MESH]|Diabetes Mellitus, Type 2/*drug therapy/physiopathology[MESH]|Dipeptidyl Peptidase 4[MESH]|Dipeptidyl-Peptidase IV Inhibitors[MESH]|Glucagon-Like Peptide-1 Receptor[MESH]|Humans[MESH]|Insulin-Secreting Cells/*cytology/drug effects[MESH]|Protease Inhibitors/therapeutic use[MESH]|Receptors, Glucagon/*physiology[MESH]|Signal Transduction[MESH] |
