PGC1alpha expression is controlled in skeletal muscles by PPARbeta, whose ablation results in fiber-type switching, obesity, and type 2 diabetes.
Détails
ID Serval
serval:BIB_1204C55A287D
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
PGC1alpha expression is controlled in skeletal muscles by PPARbeta, whose ablation results in fiber-type switching, obesity, and type 2 diabetes.
Périodique
Cell Metabolism
ISSN
1550-4131[print]
Statut éditorial
Publié
Date de publication
2006
Peer-reviewed
Oui
Volume
4
Numéro
5
Pages
407-414
Langue
anglais
Résumé
Mice in which peroxisome proliferator-activated receptor beta (PPARbeta) is selectively ablated in skeletal muscle myocytes were generated to elucidate the role played by PPARbeta signaling in these myocytes. These somatic mutant mice exhibited a muscle fiber-type switching toward lower oxidative capacity that preceded the development of obesity and diabetes, thus demonstrating that PPARbeta is instrumental in myocytes to the maintenance of oxidative fibers and that fiber-type switching is likely to be the cause and not the consequence of these metabolic disorders. We also show that PPARbeta stimulates in myocytes the expression of PGC1alpha, a coactivator of various transcription factors, known to play an important role in slow muscle fiber formation. Moreover, as the PGC1alpha promoter contains a PPAR response element, the effect of PPARbeta on the formation and/or maintenance of slow muscle fibers can be ascribed, at least in part, to a stimulation of PGC1alpha expression at the transcriptional level.
Mots-clé
Animals, Base Sequence, Cells, Cultured, Diabetes Mellitus, Type 2/etiology, Diabetes Mellitus, Type 2/metabolism, Gene Deletion, Heat-Shock Proteins/metabolism, Mice, Molecular Sequence Data, Muscle Cells/metabolism, Muscle, Skeletal/metabolism, Obesity/etiology, PPAR-beta/genetics, PPAR-beta/metabolism, Transcription Factors/metabolism
Pubmed
Web of science
Open Access
Oui
Création de la notice
24/01/2008 15:27
Dernière modification de la notice
20/08/2019 12:39