Glycogen Content Regulates Peroxisome Proliferator Activated Receptor-∂ (PPAR-∂) Activity in Rat Skeletal Muscle
Open accessAbstract
Performing exercise in a glycogen depleted state increases skeletal muscle lipid utilization and the transcription of genes regulating mitochondrial β-oxidation. Potential candidates for glycogen-mediated metabolic adaptation are the peroxisome proliferator activated receptor (PPAR) coactivator-1α (PGC-1α) and the transcription factor/nuclear receptor PPAR-∂. It was therefore the aim of the present study to examine whether acute exercise with or without glycogen manipulation affects PGC-1α and PPAR-∂ function in rodent skeletal muscle. Twenty female Wistar rats were randomly assigned to 5 experimental groups (n = 4): control [CON]; normal glycogen control [NG-C]; normal glycogen exercise [NG-E]; low glycogen control [LG-C]; and low glycogen exercise [LG-E]). Gastrocnemius (GTN) muscles were collected immediately following exercise and analyzed for glycogen content, PPAR-∂ activity via chromatin immunoprecipitation (ChIP) assays, AMPK α1/α2 kinase activity, and the localization of AMPK and PGC-1α. Exercise reduced muscle glycogen by 47 and 75% relative to CON in the NG-E and LG-E groups, respectively. Exercise that started with low glycogen (LG-E) finished with higher AMPK-α2 activity (147%, p<0.05), nuclear AMPK-α2 and PGC-1α, but no difference in AMPK-α1 activity compared to CON. In addition, PPAR-∂ binding to the CPT1 promoter was significantly increased only in the LG-E group. Finally, cell reporter studies in contracting C2C12 myotubes indicated that PPAR-∂ activity following contraction is sensitive to glucose availability, providing mechanistic insight into the association between PPAR-∂ and glycogen content/substrate availability. The present study is the first to examine PPAR-∂ activity in skeletal muscle in response to an acute bout of endurance exercise. Our data would suggest that a factor associated with muscle contraction and/or glycogen depletion activates PPAR-∂ and initiates AMPK translocation in skeletal muscle in response to exercise.
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AMPK can translocate to the nucleus where it regulates histone deacetylases, transcription factors and transcriptional co-activators such as HDAC5, MEF2 and PGC-1α.
“In a feed forward fashion AMPK can translocate to the nucleus [24,27] where it regulates Histone de-aceytlases, transcription factors and transcriptional co-activators such as histone deacetylase 5 (HDAC5), myocyte enhancing factor 2 (MEF2) and peroxisome proliferator activated receptor-γ co-activator-1α (PGC-1α) respectively (Figure 1) [28][29][30].”
From New strategies in sport nutrition to increase exercise performance (2016) · cites this paper as [24]
In rodent studies, when exercise occurs in the low glycogen state, AMPK nuclear content is increased.
“Interestingly, in rodent studies when exercise occurs in the low glycogen state AMPK nuclear content is increased [24].”
From New strategies in sport nutrition to increase exercise performance (2016) · cites this paper as [24]
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- Authors
- Philp, A., MacKenzie, M. G., Belew, M. Y., Towler, M. C., Corstorphine, A., Papalamprou, A., Hardie, D. G., & Baar, K.
- Affiliations
- University of Dundee (GB)
- University of California, Davis (US)
- Corresponding author
- Baar, Keith
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2013-10-17
- Volume
- 8
- Issue
- 10
- Pages
- e77200
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC3798319
- OpenAlex
- W2043398384
- Cited by
- 39
- References
- 44
- Citations by year
- 2022: 3 · 2021: 3 · 2020: 5 · 2019: 3 · 2018: 5 · 2017: 5 · 2016: 6 · 2015: 2 · 2014: 7
- FWCI
- 2.24
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- PLoS ONE (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Discovery Research Portal (University of Dundee) (acceptedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- eScholarship (California Digital Library) (submittedVersion)
- eScholarship (California Digital Library) (submittedVersion, cc-by)
- Funders
- Wellcome Trust (097726)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Keywords
- PPARδ, skeletal muscle glycogen, glycogen depletion, acute exercise, AMPK, PGC-1α, endurance exercise, muscle contraction, glucose availability, lipid metabolism, gastrocnemius
- MeSH terms
- Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha, Animals, Cell Line, Enzyme Activation, Female, Glucose, Glycogen, Physical Conditioning, Animal, Transcription Factors, Muscle, Skeletal, Peroxisome Proliferator-Activated Receptors, Rats, AMP-Activated Protein Kinases
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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