Retinoblastoma Protein Knockdown Favors Oxidative Metabolism and Glucose and Fatty Acid Disposal in Muscle Cells.

Détails

ID Serval
serval:BIB_8B67B071031B
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Retinoblastoma Protein Knockdown Favors Oxidative Metabolism and Glucose and Fatty Acid Disposal in Muscle Cells.
Périodique
Journal of Cellular Physiology
Auteur(s)
Petrov P.D., Ribot J., López-Mejía I.C., Fajas L., Palou A., Bonet M.L.
ISSN
1097-4652 (Electronic)
ISSN-L
0021-9541
Statut éditorial
Publié
Date de publication
2016
Peer-reviewed
Oui
Volume
231
Numéro
3
Pages
708-718
Langue
anglais
Notes
Publication types: Journal ArticlePublication Status: ppublish
Résumé
Deficiency in the retinoblastoma protein (Rb) favors leanness and a healthy metabolic profile in mice largely attributed to activation of oxidative metabolism in white and brown adipose tissues. Less is known about Rb modulation of skeletal muscle metabolism. This was studied here by transiently knocking down Rb expression in differentiated C2C12 myotubes using small interfering RNAs. Compared with control cells transfected with non-targeting RNAs, myotubes silenced for Rb (by 80-90%) had increased expression of genes related to fatty acid uptake and oxidation such as Cd36 and Cpt1b (by 61% and 42%, respectively), increased Mitofusin 2 protein content (∼2.5-fold increase), increased mitochondrial to nuclear DNA ratio (by 48%), increased oxygen consumption (by 65%) and decreased intracellular lipid accumulation. Rb silenced myotubes also displayed up-regulated levels of glucose transporter type 4 expression (∼5-fold increase), increased basal glucose uptake, and enhanced insulin-induced Akt phosphorylation. Interestingly, exercise in mice led to increased Rb phosphorylation (inactivation) in skeletal muscle as evidenced by immunohistochemistry analysis. In conclusion, the silencing of Rb enhances mitochondrial oxidative metabolism and fatty acid and glucose disposal in skeletal myotubes, and changes in Rb status may contribute to muscle physiological adaptation to exercise. J. Cell. Physiol. 231: 708-718, 2016. © 2015 Wiley Periodicals, Inc.
Pubmed
Web of science
Création de la notice
03/01/2016 17:15
Dernière modification de la notice
03/03/2018 19:11
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