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It has multiple actions including: potentiation of glucose-mediated insulin secretion mechanisms identified: increased -cell proliferation, resulting in an increase -cell mass (Fusco et al, 2017) stimulation of insulin biosynthesis at the translational level, helping to maintain -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 cells by GLP-1 increases their glucose sensitivity, resulting in less glucagon release at any glucose level (Baggio & Drucker, 2007)

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DSIP is found in both free and protein-bound forms in the hypothalamus, limbic system, and pituitary gland, as well as in peripheral organs including the gut secretory cells, pancreas (where it co-localises with glucagon), and plasma with brain and plasma DSIP concentrations showing a marked diurnal variation that correlates with circadian rhythm in humans, with levels lowest in the morning and higher in the afternoon

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