The description of the incretin effect was first described in 1964 by Elwick when he observed a greater insulin secretory response if glucose was administered orally compared to intravenously despite similar elevations in plasma glucose. This incretin effect is attributed to the release of peptide hormones from the K and L cells in the intestines in the response to eating, so that approximately 60% of the insulin subsequently secreted is related directly to the effect of incretins . Glucagon like peptide-1 (GLP-1) is secreted by the L cells, suppresses postprandial glucagon secretion, reduces appetite and stimulates insulin secretion in a dose dependent manner.
Key WordsGLP-1 analogs (incretin mimetics) Amylin analogs Incretin K and L cells Glucagon like peptide 1 (GLP-1) Postprandial glucagon secretion
- 13.Kolterman O, Kim DD, Shen L. Pharmacokinetics, pharmacodynamics and safety of exenatide in patients with type-2 diabetes mellitus. Am Health Syst Pharm. 2005;62:173–181.Google Scholar
- 18.Barnett AH, Trautmann M, Burger J, Johns D, Kim D, Brodows R, Festa A. A comparison of exenatide and insulin glargine in patients using a single oral diabetic agent. Data disclosure at the 42 annual meeting of the European Association of Diabetes. September 16, 2006.Google Scholar
- 22.Briceno RM, Lagari-Libhaber VS. Meneghini LF. Clinical observations study of the safety, effectiveness, and tolerability of exenatide in a real world setting. Diabetes. 2007;56(suppl 1):Abstract 2147-PO.Google Scholar
- 26.Victoza (liraglutide) package insert. Princeton NJ: Novo Nordisk; 2010.Google Scholar
- 36.Samsom M, Szarka LA, Camilleri M, Vella A, Zinsmeister AR, Rizza RA. Pramlintide, an amylin analog, selectively delays gastric emptying: potential role of vagal inhibition. Am J Physiol. 2000;278:G946–G951.Google Scholar