[28][29] After demonstrating its insulinotrophic properties, Dupre renamed the peptide glucose-dependent insulinotropic peptide (GIP), thus preserving the acronym.[30] Within minutes after ingestion of food, GIP is secreted from the K-cells located in the proximal region of the jejunum.[31][32][33] GIP helps maintain normal glucose homeostasis in rodent models, and has an insulinotropic effect in response to hyperglycemia in both animals and humans.[34][35][36] However, GIP does not inhibit glucagon secretion, and in fact may stimulate it during euglycemic states, and has no effect on gastric emptying.[37][38][39] Furthermore GIP concentrations in patients with type 2 diabetes are either normal, or slightly increased in response to a meal.[40][41] In patients with type 2 diabetes, GIP infusion has not been able to reduce plasma glucose concentrations, due to a lack of amplification of late phase insulin response to glucose, compared to GLP-1.[42] Thus, GIP has not been considered a suitable candidate for therapeutic development for the treatment of type 2 diabetes.[43] GLP-1 is cleaved from the proglucagon molecule by the gut specific prohormone convertase enzymes 1 and 3
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