Glucose sensing and the pathogenesis of obesity and type 2 diabetes.

Détails

ID Serval
serval:BIB_9135C1738C25
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
Titre
Glucose sensing and the pathogenesis of obesity and type 2 diabetes.
Périodique
International Journal of Obesity
Auteur(s)
Thorens B.
ISSN
1476-5497[electronic]
Statut éditorial
Publié
Date de publication
2008
Volume
32 Suppl 6
Pages
S62-S71
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't ; Review
Publication Status: ppublish
Résumé
The control of body weight and of blood glucose concentrations depends on the exquisite coordination of the function of several organs and tissues, in particular the liver, muscle and fat. These organs and tissues have major roles in the use and storage of nutrients in the form of glycogen or triglycerides and in the release of glucose or free fatty acids into the blood, in periods of metabolic needs. These mechanisms are tightly regulated by hormonal and nervous signals, which are generated by specialized cells that detect variations in blood glucose or lipid concentrations. The hormones insulin and glucagon not only regulate glycemic levels through their action on these organs and the sympathetic and parasympathetic branches of the autonomic nervous system, which are activated by glucose or lipid sensors, but also modulate pancreatic hormone secretion and liver, muscle and fat glucose and lipid metabolism. Other signaling molecules, such as the adipocyte hormones leptin and adiponectin, have circulating plasma concentrations that reflect the level of fat stored in adipocytes. These signals are integrated at the level of the hypothalamus by the melanocortin pathway, which produces orexigenic and anorexigenic neuropeptides to control feeding behavior, energy expenditure and glucose homeostasis. Work from several laboratories, including ours, has explored the physiological role of glucose as a signal that regulates these homeostatic processes and has tested the hypothesis that the mechanism of glucose sensing that controls insulin secretion by the pancreatic beta-cells is also used by other cell types. I discuss here evidence for these mechanisms, how they integrate signals from other nutrients such as lipids and how their deregulation may initiate metabolic diseases.
Mots-clé
Animals, Appetite Regulation/physiology, Blood Glucose/metabolism, Brain/metabolism, Diabetes Mellitus, Type 2/etiology, Diabetes Mellitus, Type 2/metabolism, Fatty Acids/metabolism, Glucagon/metabolism, Insulin/metabolism, Mice, Obesity/etiology, Obesity/metabolism, Pancreas/metabolism, Portal System/metabolism, Rats
Pubmed
Web of science
Open Access
Oui
Création de la notice
18/06/2009 14:19
Dernière modification de la notice
08/05/2019 22:01
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