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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Handschin, Christoph Summermatter, Serge Santos, Gesa Zorzato, Francesco Pérez-schindler, Joaquín |
| Description | Author Affiliation: Pérez-Schindler J ( Biozentrum, University of Basel, 4056 Basel, Switzerland.); |
| Abstract | Skeletal muscle mass loss and dysfunction have been linked to many diseases. Conversely, resistance exercise, mainly by activating mammalian target of rapamycin complex 1 (mTORC1), promotes skeletal muscle hypertrophy and exerts several therapeutic effects. Moreover, mTORC1, along with peroxisome proliferator-activated receptor γ coactivator 1 (PGC-1 ), regulates skeletal muscle metabolism. However, it is unclear whether PGC-1 is required for skeletal muscle adaptations after overload. Here we show that although chronic overload of skeletal muscle via synergist ablation (SA) strongly induces hypertrophy and a switch toward a slow-contractile phenotype, these effects were independent of PGC-1 . In fact, SA down-regulated PGC-1 expression and led to a repression of energy metabolism. Interestingly, however, PGC-1 deletion preserved peak force after SA. Taken together, our data suggest that PGC-1 is not involved in skeletal muscle remodeling induced by SA. |
| ISSN | 00278424 |
| e-ISSN | 10916490 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Issue Number | 50 |
| Volume Number | 110 |
| Language | English |
| Publisher | National Academy of Sciences |
| Publisher Date | 2013-12-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Energy Metabolism Physiology Multiprotein Complexes Metabolism Muscle, Skeletal TOR Serine-Threonine Kinases Transcription Factors Animals Blotting, Western DNA Primers Genetics Hypertrophy Immunohistochemistry Mice Mice, Transgenic Phosphofructokinases Polymerase Chain Reaction Succinate Dehydrogenase Research Support, Non-U.S. Gov't Multidisciplinary |
| Content Type | Text |
| Resource Type | Article |
| Subject | Multidisciplinary |
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