Glucagon-like peptide-I and the control of insulin secretion in the normal state and in NIDDM.

Détails

ID Serval
serval:BIB_D6C54D1C8031
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-I and the control of insulin secretion in the normal state and in NIDDM.
Périodique
Diabetes
Auteur(s)
Thorens B., Waeber G.
ISSN
0012-1797[print], 0012-1797[linking]
Statut éditorial
Publié
Date de publication
1993
Volume
42
Numéro
9
Pages
1219-1225
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't ; Review
Publication Status: ppublish
Résumé
Potentiation of glucose-induced insulin secretion by intestinal factors has been described for many years. Today, two major peptides with potent insulinotropic action have been recognized: gastric inhibitory peptide and truncated forms of glucagon-like peptide I, GLP-I(7-37) or the related GLP-I(7-36)amide. These hormones have specific beta-cell receptors that are coupled to production of cAMP and activation of cAMP-dependent protein kinase. Elevation in intracellular cAMP levels is required to mediate the glucoincretin effect of these hormones: the potentiation of insulin secretion in the presence of stimulatory concentrations of glucose. In addition, circulating glucoincretins maintain basal levels of cAMP, which are necessary to keep beta-cells in a glucose-competent state. Interactions between glucoincretin signaling and glucose-induced insulin secretion may result from the phosphorylation of key elements of the glucose signaling pathway by cAMP-dependent protein kinase. These include the ATP-dependent K+ channel, the Ca++ channel, or elements of the secretory machinery itself. In NIDDM, the glucoincretin effect is reduced. However, basal or stimulated gastric inhibitory peptide and glucagon-like peptide I levels are normal or even elevated, suggesting that signals induced by these hormones on the beta-cells are probably altered. At pharmacological doses, infusion of glucagon-like peptide I but not gastric inhibitory peptide, can ameliorate postprandial insulin secretory response in NIDDM patients. Agonists of the glucagon-like peptide I receptor have been proposed as new therapeutic agents in NIDDM.
Mots-clé
Animals, Cloning, Molecular, Diabetes Mellitus, Type 2/drug therapy, Diabetes Mellitus, Type 2/physiopathology, Glucagon/physiology, Glucagon/therapeutic use, Glucagon-Like Peptide 1, Glucagon-Like Peptides, Humans, Insulin/secretion, Islets of Langerhans/physiology, Peptide Fragments/physiology, Peptide Fragments/therapeutic use, Peptides/physiology, Peptides/therapeutic use, Protein Precursors/physiology, Protein Precursors/therapeutic use, Signal Transduction/physiology
Pubmed
Web of science
Création de la notice
24/01/2008 13:41
Dernière modification de la notice
20/08/2019 15:56
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