When we eat, the concentration of glucose in our blood rises due to the uptake of glucose from the digestion of starch and other carbohydrates in the gut. In healthy people, the increase is modest; eating activates other processes that
counteract any increase. One of the most important of these is the release of insulin from the beta cells in the islets of the pancreas. If the increases in blood glucose that are normally observed after a meal are mimicked by direct infusion of glucose into the blood, the amount of insulin that is secreted is much smaller than that secreted in response to the meal. This difference is due to the release of ‘incretin’ hormones from the gut which further enhance glucose-induced insulin
secretion. Jens Juul Holst reports on potential diabetes therapies based on pharmacologically enhancing or recreating the ‘incretin effect’.
incretin effect, blood sugar, glucose, post prandial hyperglycaemia, hormones, insulin, beta cell, GLP-1, GIP, glucagon-like peptide-1, islet, insulin, DPP-IV, dipeptidyl-peptidase IV, analogue, enzyme inhibitor, exenatide