|
Incretins are a group of metabolic hormones that stimulate a decrease in blood glucose levels. Incretins do so by causing an increase in the amount of insulin released from pancreatic beta cells of the islets of Langerhans after eating, before blood glucose levels become elevated. They also slow the rate of absorption of nutrients into the blood stream by reducing gastric emptying and may directly reduce food intake. As expected, they also inhibit glucagon release from the alpha cells of the islets of Langerhans. The two main candidate molecules that fulfill criteria for an incretin are the intestinal peptides glucagon-like peptide-1 (GLP-1) and gastric inhibitory peptide (also known as: glucose-dependent insulinotropic polypeptide or GIP). Both GLP-1 and GIP are rapidly inactivated by the enzyme dipeptidyl peptidase-4 (DPP-4); both GLP-1 and GIP are members of the glucagon peptide superfamily.〔(Glucagon.com ) - site of Daniel J. Drucker's laboratory that studies incretins〕 "Many factors stimulate insulin secretion, but the main one is blood glucose. Incretins, especially GIP and GLP-1 secreted, respectively, by K and L cells in the gut are also important", (Rang and Dale's Pharmacology (2015)). GLP-1 (7-36) amide is not very useful for treatment of type 2 diabetes mellitus, since it must be administered by continuous subcutaneous infusion. Several long-lasting analogs having insulinotropic activity have been developed, and three, exenatide (Byetta) and liraglutide (Victoza), plus exenatide extended-release (Bydureon), have been approved for use in the U.S. The main disadvantage of these GLP-1 analogs is they must be administered by subcutaneous injection. Another approach is to inhibit the enzyme that inactivates GLP-1 and GIP, DPP-4. Several DPP-4 inhibitors that can be taken orally as tablets have been developed. ==History== In 1902, Bayliss and Starling proposed that the intestinal mucosa contains a hormone, secretin, that stimulates the exocrine secretion of the pancreas. However, oral administration of extracts of intestinal mucosa failed to help several patients with type 1 diabetes. In 1932, La Barre proposed the name incretin for a hormone extracted from the upper gut mucosa, which caused hypoglycemia, and proposed a possible therapy for diabetes. In 1939–1940, based on their studies, Leow et al. concluded the existence of incretins was "questionable". No further research in this area was performed for about thirty years. 抄文引用元・出典: フリー百科事典『 ウィキペディア（Wikipedia）』 ■ウィキペディアで「incretin」の詳細全文を読む スポンサード リンク
|