Brown and colleagues isolated the first incretin from cholesystokinin in 1971, and named it gastric inhibitory peptide (GIP). 20,21 After demonstrating its insulinotrophic properties, Dupre renamed the peptide glucose-dependent insulinotropic peptide (GIP), thus preserving the acronym.22 Within minutes after ingestion of food, GIP is secreted from the K-cells located in the proximal region of the jejunum.23-25 GIP helps maintain normal glucose homeostasis in rodent models, and has an insulinotropic effect in response to hyperglycemia in both animals and humans.11,15,26 However, GIP does not inhibit glucagon secretion, and in fact may stimulate it during euglycemic states, and has no effect on gastric emptying.26-28 Furthermore GIP concentrations in patients with type 2 diabetes are either normal, or slightly increased in response to a meal.19,26 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-1.26 Thus, GIP has not been considered a suitable candidate for therapeutic development for the treatment of type 2 diabetes.19