Brain glucose sensing and neural regulation of insulin and glucagon secretion.

Détails

ID Serval
serval:BIB_F5B70378AC20
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Brain glucose sensing and neural regulation of insulin and glucagon secretion.
Périodique
Diabetes, Obesity and Metabolism
Auteur(s)
Thorens B.
ISSN
1463-1326 (Electronic)
ISSN-L
1462-8902
Statut éditorial
Publié
Date de publication
2011
Volume
13
Numéro
Suppl 1
Pages
82-88
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov'tPublication Status: ppublish
Résumé
Glucose homeostasis requires the tight regulation of glucose utilization by liver, muscle and white or brown fat, and glucose production and release in the blood by liver. The major goal of maintaining glycemia at ∼ 5 mM is to ensure a sufficient flux of glucose to the brain, which depends mostly on this nutrient as a source of metabolic energy. This homeostatic process is controlled by hormones, mainly glucagon and insulin, and by autonomic nervous activities that control the metabolic state of liver, muscle and fat tissue but also the secretory activity of the endocrine pancreas. Activation or inhibition of the sympathetic or parasympathetic branches of the autonomic nervous systems are controlled by glucose-excited or glucose-inhibited neurons located at different anatomical sites, mainly in the brainstem and the hypothalamus. Activation of these neurons by hyper- or hypoglycemia represents a critical aspect of the control of glucose homeostasis, and loss of glucose sensing by these cells as well as by pancreatic β-cells is a hallmark of type 2 diabetes. In this article, aspects of the brain-endocrine pancreas axis are reviewed, highlighting the importance of central glucose sensing in the control of counterregulation to hypoglycemia but also mentioning the role of the neural control in β-cell mass and function. Overall, the conclusions of these studies is that impaired glucose homeostasis, such as associated with type 2 diabetes, but also defective counterregulation to hypoglycemia, may be caused by initial defects in glucose sensing.
Pubmed
Web of science
Création de la notice
29/08/2011 7:39
Dernière modification de la notice
20/08/2019 16:22
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