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The key insulinotropic actions of GLP-1 via the class B1 G-protein-coupled receptor (GPCR) are exerted by cyclic adenosine monophosphate (cAMP) formation, which, in conjunction with increased Ca 2+ levels, promotes exocytosis of insulin-containing vesicles [39]
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In brief, SUs stimulate the release of insulin from the cells of the pancreatic islets via closure of the adenosine triphosphate (ATP)-sensitive potassium (K ATP ) channel [18]
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