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It has multiple actions including: potentiation of glucose-mediated insulin secretion mechanisms identified: increased β-cell proliferation, resulting in an increase β-cell mass (Fusco et al, 2017) stimulation of insulin biosynthesis at the translational level, helping to maintain β-cell insulin stores and secretory capacity (Baggio & Drucker, 2007) because the GLP-1 effect is glucose-dependent (there is more insulin release when glucose levels are elevated, but less effect when glucose levels are normal), GLP-1 agonists have a lower risk for producing hypoglycemia compared to sulfonylureas (that chronically stimulate insulin release, independent of glucose concentration) suppression of postprandial glucagon release Evidence indicates that stimulation of pancreatic α cells by GLP-1 increases their glucose sensitivity, resulting in less glucagon release at any glucose level (Baggio & Drucker, 2007)
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