The term incretins is used to denote intestinal hormones released in response to nutrient ingestion that are able to potentiate glucosestimulated insulin secretion.1,2 The communication between the intestine and the endocrine pancreas is demonstrated by the observation that the increase of plasma insulin levels following oral glucose administration is much greater than that seen after intravenous glucose.1–4 This phenomenon has been termed the ‘incretin effect,’ and accounts for 50–70% of the total insulin secreted after oral glucose.1–4 The first incretin hormone to be identified was gastric inhibitory polypeptide (GIP), named because of its ability to reduce gastric acid secretion in dogs. However, this effect is seen at pharmacological doses, whereas the incretin action is observed at physiological levels. The hormone was therefore re-named glucose-dependent insulinotropic polypeptide, but retains the acronym GIP.