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Activation of the GLP-1 receptor signalling pathway: a relevant strategy to repair a deficient beta-cell mass Portha B; Tourrel-Cuzin C; Movassat JExp Diabetes Res 2011[]; 2011 (ä): 376509Recent preclinical studies in rodent models of diabetes suggest that exogenous GLP-1R agonists and DPP-4 inhibitors have the ability to increase islet mass and preserve beta-cell function, by immediate reactivation of beta-cell glucose competence, as well as enhanced beta-cell proliferation and neogenesis and promotion of beta-cell survival. These effects have tremendous implication in the treatment of T2D because they directly address one of the basic defects in T2D, that is, beta-cell failure. In human diabetes, however, evidence that the GLP-1-based drugs alter the course of beta-cell function remains to be found. Several questions surrounding the risks and benefits of GLP-1-based therapy for the diabetic beta-cell mass are discussed in this review and require further investigation.|Animals[MESH]|Cell Transformation, Neoplastic/chemically induced[MESH]|Diabetes Mellitus, Type 1/*drug therapy[MESH]|Diabetes Mellitus, Type 2/*drug therapy[MESH]|Female[MESH]|Glucagon-Like Peptide-1 Receptor[MESH]|Humans[MESH]|Insulin-Secreting Cells/*drug effects/metabolism[MESH]|Middle Aged[MESH]|Pancreatic Neoplasms/chemically induced[MESH]|Pancreatitis/chemically induced[MESH]|Rats[MESH]|Receptors, Glucagon/*agonists[MESH]|Signal Transduction/*drug effects[MESH] |
