Regulator of G protein signaling-4 controls fatty acid and glucose homeostasis.

Détails

ID Serval
serval:BIB_443682EB9268
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Regulator of G protein signaling-4 controls fatty acid and glucose homeostasis.
Périodique
Endocrinology
Auteur⸱e⸱s
Iankova I., Chavey C., Clapé C., Colomer C., Guérineau N.C., Grillet N., Brunet J.F., Annicotte J.S., Fajas L.
ISSN
0013-7227 (Print)
ISSN-L
0013-7227
Statut éditorial
Publié
Date de publication
2008
Volume
149
Numéro
11
Pages
5706-5712
Langue
anglais
Résumé
Circulating free fatty acids are a reflection of the balance between lipogenesis and lipolysis that takes place mainly in adipose tissue. We found that mice deficient for regulator of G protein signaling (RGS)-4 have increased circulating catecholamines, and increased free fatty acids. Consequently, RGS4-/- mice have increased concentration of circulating free fatty acids; abnormally accumulate fatty acids in liver, resulting in liver steatosis; and show a higher degree of glucose intolerance and decreased insulin secretion in pancreas. We show in this study that RGS4 controls adipose tissue lipolysis through regulation of the secretion of catecholamines by adrenal glands. RGS4 controls the balance between adipose tissue lipolysis and lipogenesis, secondary to its role in the regulation of catecholamine secretion by adrenal glands. RGS4 therefore could be a good target for the treatment of metabolic diseases.
Mots-clé
3T3-L1 Cells, Adipose Tissue/metabolism, Animals, Cells, Cultured, Diet, Atherogenic, Fasting/blood, Fatty Acids/blood, Fatty Acids/metabolism, Fatty Liver/complications, Fatty Liver/genetics, Glucose/metabolism, Homeostasis/genetics, Hyperglycemia/complications, Hyperglycemia/genetics, Hyperinsulinism/complications, Hyperinsulinism/genetics, Insulin/secretion, Lipogenesis/genetics, Lipolysis/genetics, Mice, Mice, Knockout, RGS Proteins/genetics, RGS Proteins/physiology
Pubmed
Web of science
Open Access
Oui
Création de la notice
07/03/2013 16:01
Dernière modification de la notice
20/08/2019 13:48
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