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      Anti-diabetic actions of glucagon-like peptide-1 on pancreatic beta-cells.

      Metabolism
      Animals, Cell Differentiation, drug effects, Cell Proliferation, Cell Survival, Glucagon-Like Peptide 1, metabolism, Humans, Hypoglycemic Agents, Incretins, Insulin, biosynthesis, secretion, Insulin-Secreting Cells, Signal Transduction

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          Abstract

          Glucagon-like peptide-1 (GLP-1), an incretin hormone, is released from intestinal L-cells in response to nutrients. GLP-1 lowers blood glucose levels by stimulating insulin secretion from pancreatic beta-cells in a glucose-dependent manner. In addition, GLP-1 slows gastric emptying, suppresses appetite, reduces plasma glucagon, and stimulates glucose disposal, which are beneficial for glucose homeostasis. Therefore, incretin-based therapies such as GLP-1 receptor agonists and inhibitors of dipeptidyl peptidase IV, an enzyme which inactivates GLP-1, have been developed for treatment of diabetes. This review outlines our knowledge of the actions of GLP-1 on insulin secretion and biosynthesis, beta-cell proliferation and regeneration, and protection against beta-cell damage, as well as the involvement of recently discovered signaling pathways of GLP-1 action, mainly focusing on pancreatic beta-cells. © 2013.

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