ArticleAmerican journal of physiology. Endocrinology and metabolism2024
Disruption of hepatic mitochondrial pyruvate and amino acid metabolism impairs gluconeogenesis and endurance exercise capacity in mice.
Article in American journal of physiology. Endocrinology and metabolism, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 8 citations in OpenAlex.
- Cellular thermal shift assay of subcellular isolates to evaluate drug-membrane target interactions.MethodsX · 2026Article
- Hepatic Gluconeogenesis and the Antidepressant Effects of Exercise: A Narrative Review.Metabolites · 2026Review
- Exercise Impacts Liver Disease: Balancing Metabolic and Immune Homeostasis.International journal of biological sciences · 2026Review
- Prognostic Biomarkers for Predicting Decompensation in Alcoholic and Nonalcoholic Patients With Compensated Cirrhosis: An Umbrella Review.Biochemistry research international · 2026Review
- Exercise-Induced Molecular Adaptations in Chronic Non-Communicable Diseases-Narrative Review.International journal of molecular sciences · 2025Review
- Redox-dependent liver gluconeogenesis impacts different intensity exercise in mice.Nature metabolism · 2025Article
- Metabolic Characteristics of Obese Adolescents with Different Degrees of Weight Loss After Identical Exercise Training Intervention.Metabolites · 2025Article
- Exercise Attenuates Skeletal Muscle Atrophy in Senescent SAMP8 Mice: Metabolic Insights from NMR-Based Metabolomics.Molecules (Basel, Switzerland) · 2025Article
- Article
- Quantification of nutrient fluxes during acute exercise in mice.Cell metabolism · 2024Article
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9 authors at 4 institutions in 1 country.
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Abstract
Exercise robustly increases the glucose demands of skeletal muscle. This demand is met by not only muscle glycogenolysis but also accelerated liver glucose production from hepatic glycogenolysis and gluconeogenesis to fuel mechanical work and prevent hypoglycemia during exercise. Hepatic gluconeogenesis during exercise is dependent on highly coordinated responses within and between muscle and liver. Specifically, exercise increases the rate at which gluconeogenic precursors such as pyruvate/lactate or amino acids are delivered from muscle to the liver, extracted by the liver, and channeled into glucose. Herein, we examined the effects of interrupting hepatic gluconeogenic efficiency and capacity on exercise performance by deleting mitochondrial pyruvate carrier 2 (MPC2) and/or alanine transaminase 2 (ALT2) in the liver of mice. We found that deletion of MPC2 or ALT2 alone did not significantly affect time to exhaustion or postexercise glucose concentrations in treadmill exercise tests, but mice lacking both MPC2 and ALT2 in hepatocytes (double knockout, DKO) reached exhaustion faster and exhibited lower circulating glucose during and after exercise. Use of
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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 Socratic graph.