Glucagon-like peptide-1 and control of insulin secretion.

Détails

ID Serval
serval:BIB_E8655404BB95
Type
Article: article d'un périodique ou d'un magazine.
Sous-type
Synthèse (review): revue aussi complète que possible des connaissances sur un sujet, rédigée à partir de l'analyse exhaustive des travaux publiés.
Collection
Publications
Institution
Titre
Glucagon-like peptide-1 and control of insulin secretion.
Périodique
Diabète et Métabolisme
Auteur(s)
Thorens B.
ISSN
0338-1684[print], 0338-1684[linking]
Statut éditorial
Publié
Date de publication
12/1995
Volume
21
Numéro
5
Pages
311-318
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't ; Review
Publication Status: ppublish
Résumé
Although glucose is the major regulator of insulin secretion by pancreatic beta cells, its action is modulated by several neural and hormonal stimuli. In particular, hormones secreted by intestinal endocrine cells stimulate glucose-induced insulin secretion very potently after nutrient absorption. These hormones, called gluco-incretins or insulinotropic hormones, are major regulators of postprandial glucose homeostasis. The main gluco-incretins are GIP (gastric inhibitory polypeptide or glucose-dependent insulinotropic polypeptide) and GLP-1 (glucagon-like polypeptide-1). The secretion of GIP, a 42 amino acid polypeptide secreted by duodenal K cells, is triggered by fat and glucose. GIP stimulation of insulin secretion depends on the presence of specific beta-cell receptors and requires glucose at a concentration at least equal to or higher than the normoglycaemic level of approximately 5 mM. GIP accounts for about 50% of incretin activity, and the rest may be due to GLP-1 which is produced by proteolytic processing of the preproglucagon molecule in intestinal L cells. GLP-1 is the most potent gluco-incretin characterized so far. As with GIP, its stimulatory action requires a specific membrane receptor and normal or elevated glucose concentrations. Contrary to GIP, the incretin effect of GLP-1 is maintained in non-insulin-dependent diabetic patients. This peptide or agonists of its beta-cell receptor could provide new therapeutic tools for the treatment of Type II diabetic hyperglycaemia.
Mots-clé
Animals, Diabetes Mellitus, Type 2/physiopathology, Gastric Inhibitory Polypeptide/physiology, Glucagon/physiology, Glucagon/secretion, Glucagon-Like Peptide 1, Humans, Insulin/secretion, Peptide Fragments/physiology, Peptide Fragments/secretion, Protein Precursors/physiology, Protein Precursors/secretion, Receptors, Glucagon/chemistry, Receptors, Glucagon/metabolism, Secretory Rate/physiology, Signal Transduction/physiology
Pubmed
Web of science
Création de la notice
24/01/2008 13:41
Dernière modification de la notice
20/08/2019 16:11
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