Skeletal muscle fiber-type switching, exercise intolerance, and myopathy in PGC-1α muscle-specific knock-out animals.
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The transcriptional coactivator peroxisome proliferator-activated receptor gamma coactivator 1alpha (PGC-1alpha) is a key integrator of neuromuscular activity in skeletal muscle. Ectopic expression of PGC-1alpha in muscle results in increased mitochondrial number and function as well as an increase in oxidative, fatigue-resistant muscle fibers. Whole body PGC-1alpha knock-out mice have a very complex phenotype but do not have a marked skeletal muscle phenotype. We thus analyzed skeletal muscle-specific PGC-1alpha knock-out mice to identify a specific role for PGC-1alpha in skeletal muscle function. These mice exhibit a shift from oxidative type I and IIa toward type IIx and IIb muscle fibers. Moreover, skeletal muscle-specific PGC-1alpha knock-out animals have reduced endurance capacity and exhibit fiber damage and elevated markers of inflammation following treadmill running. Our data demonstrate a critical role for PGC-1alpha in maintenance of normal fiber type composition and of muscle fiber integrity following exertion.
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Many of these phenotypes are recapitulated in a muscle-specific PGC-1α knockout line.
“Many of these phenotypes are recapitulated in a muscle-specific PGC-1␣ knockout line (63, 64) (Table 2).”
From The role of mitochondria in the pathogenesis of type 2 diabetes (2010) · cites this paper as [63]
Muscle is significantly more insulin sensitive in both whole-body and muscle-specific PGC-1α null mice.
“Interestingly, muscle is significantly more insulin sensitive in both whole-body and muscle-specific PGC-1␣ null mice.”
From The role of mitochondria in the pathogenesis of type 2 diabetes (2010) · cites this paper as [63]
In the muscle-specific knockout lines, reduction in food intake, body weight, and adiposity may contribute to insulin sensitivity.
“In the muscle-specific knockout lines, reduction in food intake, body weight, and adiposity (despite decreased physical activity) may also contribute to insulin sensitivity (63, 64).”
From The role of mitochondria in the pathogenesis of type 2 diabetes (2010) · cites this paper as [63]
PGC-1α muscle-specific knockout results in normal mitochondrial DNA but reduced OXPHOS mRNA by 30-40% (Handschin, 2007).
“Handschin, PGC-1␣ muscle-specific Normal 30 -40% 2 mRNA | 2007 KO | (63, 64)”
From The role of mitochondria in the pathogenesis of type 2 diabetes (2010) · cites this paper as [63]
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- Authors
- Handschin, C., Chin, S., Li, P., Liu, F., Maratos-Flier, E., LeBrasseur, N. K., Yan, Z., & Spiegelman, B. M.
- Affiliations
- Harvard University (US)
- Duke Medical Center (US)
- Beth Israel Deaconess Medical Center (US)
- Boston University (US)
- Corresponding author
- Spiegelman, Bruce M.
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2007-10
- Volume
- 282
- Issue
- 41
- Pages
- 30014-30021
- ISSN
- 0021-9258 (ISSN-L)
- OpenAlex
- W2020444654
- Cited by
- 611
- References
- 31
- Citations by year
- 2026: 15 · 2025: 14 · 2024: 22 · 2023: 41 · 2022: 35 · 2021: 30 · 2020: 27 · 2019: 30 · 2018: 23 · 2017: 36 · 2016: 33 · 2015: 33 · 2014: 35 · 2013: 45 · 2012: 46
- FWCI
- 13.11
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Biological Chemistry (publishedVersion, cc-by)
- PubMed (publishedVersion)
- edoc (University of Basel) (acceptedVersion)
- Zurich Open Repository and Archive (University of Zurich) (acceptedVersion, other-oa)
- Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion, cc-by)
- Zurich Open Repository and Archive (University of Zurich) (submittedVersion, other-oa)
- Zurich Open Repository and Archive (University of Zurich)
- edoc (University of Basel)
- Funders
- National Science Foundation
- Muscular Dystrophy Association
- Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (110746)
- Universität Zürich
- National Institutes of Health (DK54477)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK54477, R01DK061562, R01DK054477, P30DK040561, DK 61562)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01AR050429, AR 050429)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Keywords
- PGC-1α, exercise intolerance, myopathy, muscle-specific knockout mice, type IIx fibers, type IIb muscle fibers, endurance capacity, muscle fiber damage, inflammation, mitochondrial function
- MeSH terms
- Animals, Glycolysis, Inflammation, Microscopy, Fluorescence, Models, Biological, Muscular Diseases, Oxygen, Physical Conditioning, Animal, Transcription Factors, Mice, Knockout, Muscle, Skeletal, Muscle Fibers, Fast-Twitch, Muscle Fibers, Slow-Twitch, Mice
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