ArticleExperimental physiology2013
Effect of exercise on mouse liver and brain bioenergetic infrastructures.
Article in Experimental physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 47 citations in OpenAlex.
- Exercise Resistance in Obese Male NZO Mice Manifests as Local Muscle Remodelling Without Glycaemic Improvements.Diabetes, obesity & metabolism · 2026Article
- The inhibition of lactate/Gpr81 signalling driven by moderate-intensity continuous training protects against osteoarthritis.Experimental & molecular medicine · 2026Article
- Regular versus Irregular Exercise Differentially Modulates Hippocampal-Hepatic Acetylcholine Flux to Coordinate Fear Memory Extinction and Liver Inflammation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The Neurometabolic Function of the Dopamine-Aminotransferase System.Metabolites · 2025Review
- The mitochondrial quality control system: a new target for exercise therapeutic intervention in the treatment of brain insulin resistance-induced neurodegeneration in obesity.International journal of obesity (2005) · 2024Review
- Chronic exercise improves hepatic acylcarnitine handling.iScience · 2024Article
- Enhanced glucose production in norepinephrine and palmitate stimulated hepatocytes following endurance training.Frontiers in physiology · 2024Article
- Induced Coma, Death, and Organ Transplantation: A Physiologic, Genetic, and Theological Perspective.International journal of molecular sciences · 2023Review
- Swimming exercise is a promising early intervention for autism-like behavior in Shank3 deletion rats.CNS neuroscience & therapeutics · 2023Article
- AMPK and the Adaptation to Exercise.Annual review of physiology · 2022Review
- Proteomic analysis of the effect of high-fat-diet and voluntary physical activity on mouse liver.PloS one · 2022Article
- Exercise alters the mitochondrial proteostasis and induces the mitonuclear imbalance and UPRScientific reports · 2021Article
- Physical exercise and liver "fitness": Role of mitochondrial function and epigenetics-related mechanisms in non-alcoholic fatty liver disease.Molecular metabolism · 2020Review
- Article
- Ultra-Endurance Associated With Moderate Exercise in Rats Induces Cerebellar Oxidative Stress and Impairs Reactive GFAP Isoform Profile.Frontiers in molecular neuroscience · 2020Article
- The host response to poly(lactide-co-glycolide) scaffolds protects mice from diet induced obesity and glucose intolerance.Biomaterials · 2019Article
- Endurance training slows breast tumor growth in mice by suppressing Treg cells recruitment to tumors.BMC cancer · 2019Article
- Pros and cons of insulin administration on liver glucose metabolism in strength-trained healthy mice.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2019Article
- Relationships Between Mitochondria and Neuroinflammation: Implications for Alzheimer's Disease.Current topics in medicinal chemistry · 2016Review
- Head to Head Comparison of Short-Term Treatment with the NAD(+) Precursor Nicotinamide Mononucleotide (NMN) and 6 Weeks of Exercise in Obese Female Mice.Frontiers in pharmacology · 2016Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
To assess the effects of exercise on liver and brain bioenergetic infrastructures, we exposed C57BL/6 mice to 6 weeks of moderate-intensity treadmill exercise. During the training period, fasting blood glucose was lower in exercised mice than in sedentary mice, but serum insulin levels were not reduced. At week 6, trained mice showed a paradoxical decrease in plasma lactate during exercise, which was accompanied by an increase in the liver monocarboxylate transporter 2 protein level (∼30%, P < 0.05). Exercise increased liver peroxisomal proliferator-activated receptor-γ coactivator 1α expression (approximately twofold, P < 0.001), NAD-dependent deacetylase sirtuin-1 protein (∼30%, P < 0.05), p38 protein (∼15%, P < 0.05), cytochrome c oxidase subunit 4 isoform 1 protein (∼50%, P < 0.05) and AMP-activated protein kinase phosphorylation (∼40%, P < 0.05). Despite this, liver mitochondrial DNA copy number (∼30%, P = 0.05), mitochondrial transcription factor A expression (∼15%, P < 0.05), cytochrome c oxidase subunit 2 expression (∼10%, P < 0.05), cAMP-response element binding protein phosphorylation (∼60%, P < 0.05) and brain-derived neurotrophic factor expression (∼40%, P < 0.05) were all reduced, while cytochrome oxidase and citrate synthase activities were unchanged. The only altered brain parameter observed was a reduction in tumour necrosis factor α expression (∼35%, P < 0.05); tumour necrosis factor α expression was unchanged in liver. Our data suggest that lactate produced by exercising muscle modifies the liver bioenergetic infrastructure, and enhanced liver uptake may in turn limit the ability of exercise-generated lactate to modify brain bioenergetics. Also, it appears that, at least in the liver, a dissociated mitochondrial biogenesis, in which some components are strategically enhanced while others are minimized, can occur.
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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.