ArticleGenes & development2011
The nuclear receptor PPARβ/δ programs muscle glucose metabolism in cooperation with AMPK and MEF2.
Article in Genes & development, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.
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Who cites it
78 citing papers in PubMed, 134 citations in OpenAlex.
- Epigenetic Modulation of Exercise Adaptation: The Role of Dietary Supplementation in Athletic Performance.Genes · 2026Review
- BRD4 directs myofiber identity and metabolic adaptation through CHD4 cooperation.Nature communications · 2026Article
- Enhancer regulator MLL4 controls skeletal muscle metabolic efficiency by limiting AMPK-mediated fuel catabolism.Nature communications · 2025Article
- A role for the transcriptional coregulator RIP140 in the control of muscle endurance fitness.JCI insight · 2025Article
- Uncoupling protein 3 regulates energy and stress-related pathways in undifferentiated skeletal muscle myoblasts.American journal of physiology. Cell physiology · 2025Article
- Nicotinamide phosphoribosyltransferase (Nampt) in Lateral Hypothalamus Maintains Skeletal Muscle Functions Through Lactate-Mediated Calcium Signalling in Male Mice.Journal of cachexia, sarcopenia and muscle · 2025Article
- Impact of exercise and fasting on mitochondrial regulators in human muscle.Translational exercise biomedicine · 2024Article
- Eicosapentaenoic acid increases proportion of type 1 muscle fibers through PPARδ and AMPK pathways in rats.iScience · 2024Article
- The Acute, Short-, and Long-Term Effects of Endurance Exercise on Skeletal Muscle Transcriptome Profiles.International journal of molecular sciences · 2024Article
- AMPK phosphorylation of FNIP1 (S220) controls mitochondrial function and muscle fuel utilization during exercise.Science advances · 2024Article
- Remodeling of the human skeletal muscle proteome found after long-term endurance training but not after strength training.iScience · 2024Article
- DNA hypomethylation characterizes genes encoding tissue-dominant functional proteins in liver and skeletal muscle.Scientific reports · 2023Article
- Nuclear receptors as potential therapeutic targets in peripheral arterial disease and related myopathy.The FEBS journal · 2023Review
- Transcriptional control of energy metabolism by nuclear receptors.Nature reviews. Molecular cell biology · 2022Review
- Review
- Pathogenesis and Therapeutic Strategies Related to Non-Alcoholic Fatty Liver Disease.International journal of molecular sciences · 2022Review
- Fimasartan Ameliorates Deteriorations in Glucose Metabolism in a High Glucose State by Regulating Skeletal Muscle and Liver Cells.Yonsei medical journal · 2022Article
- Enhancement of anaerobic glycolysis - a role of PGC-1α4 in resistance exercise.Nature communications · 2022Article
- Disuse-associated loss of the protease LONP1 in muscle impairs mitochondrial function and causes reduced skeletal muscle mass and strength.Nature communications · 2022Article
- Role of Peroxisome Proliferator-Activated Receptors (PPARs) in Energy Homeostasis of Dairy Animals: Exploiting Their Modulation through Nutrigenomic Interventions.International journal of molecular sciences · 2021Review
18 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
To identify new gene regulatory pathways controlling skeletal muscle energy metabolism, comparative studies were conducted on muscle-specific transgenic mouse lines expressing the nuclear receptors peroxisome proliferator-activated receptor α (PPARα; muscle creatine kinase [MCK]-PPARα) or PPARβ/δ (MCK-PPARβ/δ). MCK-PPARβ/δ mice are known to have enhanced exercise performance, whereas MCK-PPARα mice perform at low levels. Transcriptional profiling revealed that the lactate dehydrogenase b (Ldhb)/Ldha gene expression ratio is increased in MCK-PPARβ/δ muscle, an isoenzyme shift that diverts pyruvate into the mitochondrion for the final steps of glucose oxidation. PPARβ/δ gain- and loss-of-function studies in skeletal myotubes demonstrated that PPARβ/δ, but not PPARα, interacts with the exercise-inducible kinase AMP-activated protein kinase (AMPK) to synergistically activate Ldhb gene transcription by cooperating with myocyte enhancer factor 2A (MEF2A) in a PPARβ/δ ligand-independent manner. MCK-PPARβ/δ muscle was shown to have high glycogen stores, increased levels of GLUT4, and augmented capacity for mitochondrial pyruvate oxidation, suggesting a broad reprogramming of glucose utilization pathways. Lastly, exercise studies demonstrated that MCK-PPARβ/δ mice persistently oxidized glucose compared with nontransgenic controls, while exhibiting supranormal performance. These results identify a transcriptional regulatory mechanism that increases capacity for muscle glucose utilization in a pattern that resembles the effects of exercise training.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.