The DOI matches its Crossref record; 69 of the 69 references it cites were found in a registry or an index.
A role for the transcriptional coactivator PGC-1α in muscle refueling.
Open accessAbstract
The transcriptional coactivator peroxisome proliferator-activated receptor gamma coactivator-1alpha (PGC-1alpha) has been identified as an inducible regulator of mitochondrial function. Skeletal muscle PGC-1alpha expression is induced post-exercise. Therefore, we sought to determine its role in the regulation of muscle fuel metabolism. Studies were performed using conditional, muscle-specific, PGC-1alpha gain-of-function and constitutive, generalized, loss-of-function mice. Forced expression of PGC-1alpha increased muscle glucose uptake concomitant with augmentation of glycogen stores, a metabolic response similar to post-exercise recovery. Induction of muscle PGC-1alpha expression prevented muscle glycogen depletion during exercise. Conversely, PGC-1alpha-deficient animals exhibited reduced rates of muscle glycogen repletion post-exercise. PGC-1alpha was shown to increase muscle glycogen stores via several mechanisms including stimulation of glucose import, suppression of glycolytic flux, and by down-regulation of the expression of glycogen phosphorylase and its activating kinase, phosphorylase kinase alpha. These findings identify PGC-1alpha as a critical regulator of skeletal muscle fuel stores.
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“By contrast, highlevel overexpression of PGC-1␣ may actually reduce insulin sensitivity via reduced glycolysis and/or glucose oxidation (265) or myofibrillar disruption/myopathy, potentially limiting exercise tolerance.”
From The role of mitochondria in the pathogenesis of type 2 diabetes (2010) · cites this paper as [265]
In the citing paper
“In these animals, both muscle glucose uptake and glycogen deposition were increased.”
From The role of mitochondria in the pathogenesis of type 2 diabetes (2010) · cites this paper as [265]
In the citing paper
“Inducible overexpression of PGC-1␣ in skeletal muscle ( 265) results in increased mitochondrial density and a robust increase in expression of OXPHOS genes and genes necessary for fatty acid oxidation.”
From The role of mitochondria in the pathogenesis of type 2 diabetes (2010) · cites this paper as [265]
In the citing paper
“Although low-intensity exercise performance did not differ in this model, high-performance exercise was impaired, in parallel with failure to mobilize stored glycogen.”
From The role of mitochondria in the pathogenesis of type 2 diabetes (2010) · cites this paper as [265]
Citations
Cites
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Transcriptional co-activator PGC-1α drives the formation of slow-twitch muscle fibres
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Cited by
Sorted by citations
Exercise Metabolism and the Molecular Regulation of Skeletal Muscle Adaptation
Egan, B., & Zierath, J. R. (2013) · Cell Metabolism · doi:10.1016/j.cmet.2012.12.012 · Cited by 2,084
“In muscle-specific PGC-1a KO mice,many of these adaptations are reversed, e.g.,muscle fibers exhibit a more glycolytic phenotype, impaired mitochondrial respiratory function, reduced exercise capacity, and impaired recovery from exercise (Handschin et al., 2007; Wende et al., 2007).”
BackgroundThe role of exercise and PGC1α in inflammation and chronic disease
Handschin, C., & Spiegelman, B. M. (2008) · Nature · doi:10.1038/nature07206 · Cited by 1,083
“The fibre switch promoted by PGC1α in these mice is characterized by an increase in mitochondrial density and function, an increase in oxidative metabolism, an increase in expression of myofibrillar proteins that are characteristic of type I and type IIA muscle fibres, and a switch in substrate fuel usag”
A PGC-1α isoform induced by resistance training regulates skeletal muscle hypertrophy
Ruas, J. L., White, J. P., Rao, R. R., Kleiner, S., Brannan, K. T., Harrison, B. C., Greene, N. P., Wu, J., Estall, J. L., Irving, B. A., et al. (2012) · Cell · doi:10.1016/j.cell.2012.10.050 · Cited by 677
“However, gain-of-function studies with PGC1a have not shown any increase in either muscle mass or strength (Lin et al., 2002; Sandri et al., 2006; Wende et al., 2007).”
Little, J. P., Safdar, A., Wilkin, G. P., Tarnopolsky, M. A., & Gibala, M. J. (2010) · The Journal of Physiology · doi:10.1113/jphysiol.2009.181743 · Cited by 708
“The regulation of skeletal muscle glycogen content by PGC-1α is not completely understood, but may involve PGC-1α mediated up-regulation of GLUT4 (Michael et al. 2001) and/or modulation of enzymes involved in glycogen synthesis and degradation (Wende et al. 2007).”
BackgroundInfluentialBentzinger, C. F., Romanino, K., Cloëtta, D., Lin, S., Mascarenhas, J. B., Oliveri, F., Xia, J., Casanova, E., Costa, C. F., Brink, M., et al. (2008) · Cell Metabolism · doi:10.1016/j.cmet.2008.10.002 · Cited by 640
Metadata
- Authors
- Wende, A. R., Schaeffer, P. J., Parker, G. J., Zechner, C., Han, D.-H., Chen, M. M., Hancock, C. R., Lehman, J. J., Huss, J. M., McClain, D. A., Holloszy, J. O., & Kelly, D. P.
- Affiliations
- Washington University in St. Louis (US)
- University of Utah (US)
- Corresponding author
- Kelly, Daniel P.
- ORCID
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2007-12
- Volume
- 282
- Issue
- 50
- Pages
- 36642-36651
- ISSN
- 0021-9258 (ISSN-L)
- OpenAlex
- W2130246533
- Cited by
- 257
- References
- 69
- Citations by year
- 2026: 2 · 2025: 8 · 2024: 5 · 2023: 6 · 2022: 7 · 2021: 9 · 2020: 10 · 2019: 10 · 2018: 15 · 2017: 18 · 2016: 14 · 2015: 10 · 2014: 26 · 2013: 23 · 2012: 17
- FWCI
- 13.42
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Biological Chemistry (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5p60dk020579-35)
- National Institute on Aging (R01AG000425)
- National Heart, Lung, and Blood Institute (T32HL007275)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK045416, P60-DK-020579, P30DK056341, P30DK052574, R01DK074700)
- Topics
- Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Keywords
- PGC-1α, glycogen stores, glucose uptake, post-exercise recovery, mitochondrial biogenesis, glycogen phosphorylase, glycolytic flux, glucose transport
- MeSH terms
- Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha, Animals, Glucose, Glycogen, Mice, Transgenic, Mitochondria, Muscle, Muscle Proteins, Phosphorylase Kinase, Transcription Factors, Trans-Activators, Muscle, Skeletal, Glycogen Phosphorylase, Mice
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