The DOI matches its Crossref record; 45 of the 45 references it cites were found in a registry or an index.
Total Skeletal Muscle PGC-1 Deficiency Uncouples Mitochondrial Derangements from Fiber Type Determination and Insulin Sensitivity
Open accessAbstract
Evidence is emerging that the PGC-1 coactivators serve a critical role in skeletal muscle metabolism, function, and disease. Mice with total PGC-1 deficiency in skeletal muscle (PGC-1α(-/-)β(f/f/MLC-Cre) mice) were generated and characterized. PGC-1α(-/-)β(f/f/MLC-Cre) mice exhibit a dramatic reduction in exercise performance compared to single PGC-1α- or PGC-1β-deficient mice and wild-type controls. The exercise phenotype of the PGC-1α(-/-)β(f/f/MLC-Cre) mice was associated with a marked diminution in muscle oxidative capacity, together with rapid depletion of muscle glycogen stores. In addition, the PGC-1α/β-deficient muscle exhibited mitochondrial structural derangements consistent with fusion/fission and biogenic defects. Surprisingly, the proportion of oxidative muscle fiber types (I, IIa) was not reduced in the PGC-1α(-/-)β(f/f/MLC-Cre) mice. Moreover, insulin sensitivity and glucose tolerance were not altered in the PGC-1α(-/-)β(f/f/MLC-Cre) mice. Taken together, we conclude that PGC-1 coactivators are necessary for the oxidative and mitochondrial programs of skeletal muscle but are dispensable for fundamental fiber type determination and insulin sensitivity.
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“Along the same line, insulin-stimulated glucose sensitivity is increased in some mouse models of mitochondrial dysfunction (Wredenberg et al, 2006; Pospisilik et al, 2007; Zechner et al, 2010).”
From Mitochondrial response to nutrient availability and its role in metabolic disease (2014) · cites this paper as Zechner et al, 2010
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1 retracted
Wenz, T., Rossi, S. G., Rotundo, R. L., Spiegelman, B. M., & Moraes, C. T. (2009) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0911570106 · Cited by 600 · cited 2×
“PGC-1 overexpression in mice has been shown to inhibit the protein degradation known to occur in disuse atrophy (Wenz et al., 2009; Brault et al., 2010).”
BackgroundRetractedMootha, V. K., Lindgren, C. M., Eriksson, K.-F., Subramanian, A., Sihag, S., Lehar, J., Puigserver, P., Carlsson, E., Ridderstråle, M., Laurila, E., et al. (2003) · Nature Genetics · doi:10.1038/ng1180 · Cited by 10,197
Wu, Z., Puigserver, P., Andersson, U., Zhang, C., Adelmant, G., Mootha, V., Troy, A., Cinti, S., Lowell, B., Scarpulla, R. C., et al. (1999) · Cell · doi:10.1016/s0092-8674(00)80611-x · Cited by 4,139 · cited 4×
“Interest- ingly, expression of the gene encoding nuclear respiratory factor 1 (NRF-1), a PGC-1a target (Wu et al., 1999) involved in regu- lating OXPHOS genes and coordinating nuclear and mitochon- drial genomes, was similar among the groups.”
BackgroundInfluentialA Cold-Inducible Coactivator of Nuclear Receptors Linked to Adaptive Thermogenesis
Puigserver, P., Wu, Z., Park, C. W., Graves, R., Wright, M., & Spiegelman, B. M. (1998) · Cell · doi:10.1016/s0092-8674(00)81410-5 · Cited by 3,864 · cited 2×
“Originally discovered in brown adipose tissue (Puigserver et al., 1998), PGC-1a enhances transcription by interacting directly with target transcription factors, including PPARg and other members of the nuclear receptor superfamily (reviewed in”
BackgroundTranscriptional co-activator PGC-1α drives the formation of slow-twitch muscle fibres
Lin, J., Wu, H., Tarr, P. T., Zhang, C.-Y., Wu, Z., Boss, O., Michael, L. F., Puigserver, P., Isotani, E., Olson, E. N., et al. (2002) · Nature · doi:10.1038/nature00904 · Cited by 2,546 · cited 3×
“Plasma free fatty acids were also determined by a colorimetric assay (Lin et al., 2002b).”
BackgroundMethodMetabolic control through the PGC-1 family of transcription coactivators
Lin, J., Handschin, C., & Spiegelman, B. M. (2005) · Cell Metabolism · doi:10.1016/j.cmet.2005.05.004 · Cited by 2,130 · cited 2×
“The transcriptional coactivators PPARg coactivator-1a (PGC-1a) and PGC-1b serve as regulators of mitochondrial biogenesis and cellular energy metabolism (Kelly and Scarpulla, 2004; Lin et al., 2005).”
BackgroundMitochondrial dysfunction and type 2 diabetes
Lowell, B. B., & Shulman, G. I. (2005) · Science · doi:10.1126/science.1104343 · Cited by 2,070
Patti, M. E., Butte, A. J., Crunkhorn, S., Cusi, K., Berria, R., Kashyap, S., Miyazaki, Y., Kohane, I., Costello, M., Saccone, R., et al. (2003) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1032913100 · Cited by 1,952 · cited 4×
“In addition, several studies in humans have shown reduced expression of PGC-1a (Mootha et al., 2003; Patti et al., 2003) in skeletal muscle of insulin-resistant and diabetic subjects.”
BackgroundInfluentialPGC-1 coactivators: inducible regulators of energy metabolism in health and disease
Finck, B. N. (2006) · Journal of Clinical Investigation · doi:10.1172/jci27794 · Cited by 1,461 · cited 3×
“…discovered in brown adipose tissue (Puigserver et al., 1998), PGC-1a enhances transcription by interacting directly with target transcription factors, including PPARg and other members of the nuclear receptor superfamily (reviewed in Cell M Finck and Kelly, 2006; Handschin and Spiegelman, 2006).”
BackgroundDisruption of Fusion Results in Mitochondrial Heterogeneity and Dysfunction
Chen, H., Chomyn, A., & Chan, D. C. (2005) · Journal of Biological Chemistry · doi:10.1074/jbc.m503062200 · Cited by 1,376 · cited 2×
“This latter function has been ascribed to the ongoing dynamics of fusion and fission, which serve to maintain mitochondrial quality control (Chen et al., 2005; Waterham et al., 2007; Zhang and Chan, 2007).”
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Mechanisms of Insulin Action and Insulin Resistance
Petersen, M. C., & Shulman, G. I. (2018) · Physiological Reviews · doi:10.1152/physrev.00063.2017 · Cited by 3,028
Sarcopenia: Aging-Related Loss of Muscle Mass and Function
Larsson, L., Degens, H., Li, M., Salviati, L., Lee, Y. I., Thompson, W., Kirkland, J. L., & Sandri, M. (2019) · Physiological Reviews · doi:10.1152/physrev.00061.2017 · Cited by 1,797
Gomes, A. P., Price, N. L., Ling, A. J. Y., Moslehi, J. J., Montgomery, M. K., Rajman, L., White, J. P., Teodoro, J. S., Wrann, C. D., Hubbard, B. P., et al. (2013) · Cell · doi:10.1016/j.cell.2013.11.037 · Cited by 1,482
“To test this, we examined primary myotubes from PGC-1a/b knockout (KO) mice (Zechner et al., 2010) and from PGC-1a muscle-specific null mice (Handschin et al.”
MethodAustin, S., & St‐Pierre, J. (2012) · Journal of Cell Science · doi:10.1242/jcs.113662 · Cited by 617
Mammalian Mitochondria and Aging: An Update
Kauppila, T. E. S., Kauppila, J. H. K., & Larsson, N.-G. (2017) · Cell Metabolism · doi:10.1016/j.cmet.2016.09.017 · Cited by 578
“…of Pgc1a in mice leads to muscle fiber type switching from fast-twitching glycolytic fibers to slow-twitching oxidative fibers (Lin et al., 2002), it is still unclear how important PGC1a is for muscle fiber type determination in wild-type mice (Handschin et al., 2007; Zechner et al., 2010).”
Metadata
- Authors
- Zechner, C., Lai, L., Zechner, J. F., Geng, T., Yan, Z., Rumsey, J. W., Collia, D., Chen, Z., Wozniak, D. F., Leone, T. C., & Kelly, D. P.
- Affiliations
- Sanford Burnham Prebys Medical Discovery Institute (US)
- University of Virginia Medical Center (US)
- Washington University in St. Louis (US)
- Corresponding author
- Kelly, Daniel P.
- ORCID
- Venue
- Cell Metabolism
- Publisher
- Elsevier BV
- Published
- 2010-12
- Volume
- 12
- Issue
- 6
- Pages
- 633-642
- ISSN
- 1550-4131 (ISSN-L)
- PMC
- PMC2999961
- OpenAlex
- W2064754499
- Cited by
- 274
- References
- 45
- Citations by year
- 2026: 4 · 2025: 18 · 2024: 11 · 2023: 12 · 2022: 19 · 2021: 13 · 2020: 13 · 2019: 19 · 2018: 19 · 2017: 21 · 2016: 23 · 2015: 22 · 2014: 12 · 2013: 31 · 2012: 16
- FWCI
- 14.73
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 959 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Cell Metabolism (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (DK45416, HL58427, P30 NS057105)
- American Diabetes Association (AR050429)
- Washington University School of Medicine in St. Louis
- Deutsche Forschungsgemeinschaft (ZE 796/2-1)
- Topics
- Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Keywords
- PGC-1α, PGC-1β, skeletal muscle, mitochondrial dysfunction, mitochondrial fission and fusion, oxidative capacity, muscle glycogen depletion, exercise performance, insulin sensitivity, glucose tolerance, muscle metabolism
- MeSH terms
- Analysis of Variance, Animals, Glucose Tolerance Test, Insulin Resistance, Microscopy, Electron, Mitochondria, Oxygen Consumption, Physical Conditioning, Animal, Transcription Factors, Polymerase Chain Reaction, Mice, Knockout, Muscle, Skeletal, Gene Expression Profiling, Mice
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