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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)

Reduced food intake means less dietary iron

Pharmacologic approaches to glycemic treatment: standards of medical Care in diabetes2021

From My Medical Studies In our physiology classes, we study both GLP-1 and GIP as the two main incretin hormones responsible for the incretin effect the phenomenon where oral glucose causes a much greater insulin response than intravenous glucose

Interestingly, DPP4 expression was found to be higher in synovial fluid T cells in osteoarthritis patients than in RA patients