ABSTRACT
Early in the first half of the 20th century it was already hypothesized that gastrointestinal hormones are important for glucose homeostasis and stimulation of insulin secretion after a meal (1,2). In the late 1960s it was finally shown that orally administered glucose leads to a greater insulin response than intravenously administered glucose dosed to lead to identical serum glucose excursions (3). This difference in insulin secretion is termed the “incretin effect.” The gastrointestinal hormones promoting the pronounced insulin response after an oral glucose load are called “incretins.” The incretin effect is responsible for approximately 30% to 60% of the postprandial C-peptide response depending on the amount of glucose consumed. In patients with type 2 diabetes the incretin effect is markedly reduced (4,5).
