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Glucagon-like peptide 1 is a gastrointestinally derived hormone with profound effects on nutrient-induced pancreatic hormone release. GLP-1 modulates insulin, glucagon and somatostatin secretion by binding to guanine nucleotide binding protein-coupled receptors resulting in the activation of adenylate cyclase and generation of cyclic adenosine monophosphate (cAMP). In the B-cell, cAMP, via activation of protein kinase A, interacts with a plethora of signal transduction processes including ion channel activity, intracellular Ca2+ handling and exocytosis of the insulin-containing granules. The stimulatory action of GLP-1 on insulin secretion, contrary to that of the currently used hypoglycaemic sulphonylureas, is glucose dependent and requires the presence of normal or elevated concentrations of the sugar. For this reason, GLP-1 attracts much interest as a possible novel principle for the treatment of human type-2 diabetes. Here we review the actions of GLP-1 on islet cell function and attempt to integrate current knowledge into a working model for the control of pancreatic hormone secretion.

Original publication

DOI

10.1007/s004240050558

Type

Journal article

Journal

Pflugers Arch

Publication Date

04/1998

Volume

435

Pages

583 - 594

Keywords

Animals, Calcium, Diabetes Mellitus, Type 2, Exocytosis, Glucagon, Glucagon-Like Peptide 1, Glucagon-Like Peptide-1 Receptor, Glucagon-Like Peptides, Humans, Ion Channels, Islets of Langerhans, Pancreatic Hormones, Peptide Fragments, Protein Precursors, Receptors, Glucagon