Document Detail

Mitofusins 1/2 and ERRalpha expression are increased in human skeletal muscle after physical exercise.
MedLine Citation:
PMID:  15961417     Owner:  NLM     Status:  MEDLINE    
Mitochondrial impairment is hypothesized to contribute to the pathogenesis of insulin resistance. Mitofusin (Mfn) proteins regulate the biogenesis and maintenance of the mitochondrial network, and when inactivated, cause a failure in the mitochondrial architecture and decreases in oxidative capacity and glucose oxidation. Exercise increases muscle mitochondrial content, size, oxidative capacity and aerobic glucose oxidation. To address if Mfn proteins are implicated in these exercise-induced responses, we measured Mfn1 and Mfn2 mRNA levels, pre-, post-, 2 and 24 h post-exercise. Additionally, we measured the expression levels of transcriptional regulators that control mitochondrial biogenesis and functions, including PGC-1alpha, NRF-1, NRF-2 and the recently implicated ERRalpha. We show that Mfn1, Mfn2, NRF-2 and COX IV mRNA were increased 24 h post-exercise, while PGC-1alpha and ERRalpha mRNA increased 2 h post-exercise. Finally, using in vitro cellular assays, we demonstrate that Mfn2 gene expression is driven by a PGC-1alpha programme dependent on ERRalpha. The PGC-1alpha/ERRalpha-mediated induction of Mfn2 suggests a role of these two factors in mitochondrial fusion. Our results provide evidence that PGC-1alpha not only mediates the increased expression of oxidative phosphorylation genes but also mediates alterations in mitochondrial architecture in response to aerobic exercise in humans.
Romain Cartoni; Bertrand Léger; M Benjamin Hock; Manu Praz; Antoinette Crettenand; Sara Pich; Jean-Luc Ziltener; François Luthi; Olivier Dériaz; Antonio Zorzano; Charles Gobelet; Anastasia Kralli; Aaron P Russell
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.     Date:  2005-06-16
Journal Detail:
Title:  The Journal of physiology     Volume:  567     ISSN:  0022-3751     ISO Abbreviation:  J. Physiol. (Lond.)     Publication Date:  2005 Aug 
Date Detail:
Created Date:  2005-08-17     Completed Date:  2005-11-01     Revised Date:  2011-12-19    
Medline Journal Info:
Nlm Unique ID:  0266262     Medline TA:  J Physiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  349-58     Citation Subset:  IM    
Clinique Romande de Réadaptation, SUVACare, 1951 Sion, Switzerland.
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MeSH Terms
Energy Metabolism / physiology
Estrogen Receptor alpha / genetics*
Exercise / physiology*
GTP Phosphohydrolases / genetics*
Gene Expression / physiology
Membrane Proteins / genetics
Membrane Transport Proteins / genetics*
Mitochondria / physiology
Mitochondrial Membrane Transport Proteins
Mitochondrial Proteins / genetics*
Muscle, Skeletal / physiology*
Promoter Regions, Genetic / physiology
Signal Transduction / physiology
Grant Support
Reg. No./Substance:
0/Estrogen Receptor alpha; 0/Membrane Proteins; 0/Membrane Transport Proteins; 0/Mitochondrial Membrane Transport Proteins; 0/Mitochondrial Proteins; EC 3.6.1.-/GTP Phosphohydrolases; EC 3.6.1.-/MFN2 protein, human; EC 3.6.5.-/Mfn1 protein, human

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