ArticleInternational journal of molecular sciences2022
Long-Chain and Medium-Chain Fatty Acids in Energy Metabolism of Murine Kidney Mitochondria.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 30 citations in OpenAlex.
- Tubular ACSM3 controls fatty acid metabolism and safeguards against acute kidney injury in male mice.Nature communications · 2026Article
- Sex-dependent differences in mitochondrial protein acetylation in metabolic condition, oxidative stress, vascular dysfunction, hypertension, and cardiovascular disease.Clinical science (London, England : 1979) · 2026Review
- Energy metabolism, adenosine, and glutamate signaling reprogramming by decanoic acid in Glut1 disorder syndrome.Epilepsia open · 2026Article
- Spatial metabolomics: A new tool for unravelling the metabolic disorders and heterogeneity in diabetic kidney disease (Review).International journal of molecular medicine · 2026Review
- Rethinking Human Energy Metabolism.Current issues in molecular biology · 2026Review
- MCJ modulates mitochondrial ETC flux to promote lipid metabolism-driven enhancement of cell proliferation and migration.Cell death & disease · 2026Article
- Bioenergetic profiles and respiratory control in mitochondrial physiology: Precision analysis of oxidative phosphorylation.Experimental physiology · 2026Article
- Associations Between Gestational Diabetes Mellitus and Neonatal Acyl Metabolic Profiles: An Empirical Study Based on a Birth Cohort.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Article
- Epigenetic Histone β-Hydroxybutyrylation Contributes to Renoprotection by β-Hydroxybutyrate in the Dahl Rat.Hypertension (Dallas, Tex. : 1979) · 2025Article
- Phylogenetic Aspects of Higher Plant Lipid Fatty Acid Profile.International journal of molecular sciences · 2025Review
- Uncovering potential biomarkers and metabolic pathways in systemic lupus erythematosus and lupus nephritis through integrated microbiome and metabolome analysis.BMC microbiology · 2025Article
- Ketone body mediated histone β-hydroxybutyrylation is reno-protective.bioRxiv : the preprint server for biology · 2025Article
- The Importance of Mitochondrial Processes in the Maturation and Acquisition of Competences of Oocytes and Embryo Culture.International journal of molecular sciences · 2025Review
- The Pathogenesis of Very Long-Chain Acyl-CoA Dehydrogenase Deficiency.Biomolecules · 2025Review
- Targeting Mitochondrial Dysfunction in Cerebral Ischemia: Advances in Pharmacological Interventions.Antioxidants (Basel, Switzerland) · 2025Review
- Role of Fatty Acids β-Oxidation in the Metabolic Interactions Between Organs.International journal of molecular sciences · 2024Review
- Plasmalogens and Octanoylcarnitine Serve as Early Warnings for Central Retinal Artery Occlusion.Molecular neurobiology · 2024Article
- Critical Role of Mitochondrial Fatty Acid Metabolism in Normal Cell Function and Pathological Conditions.International journal of molecular sciences · 2024Review
- Mitochondrial CypD Acetylation Promotes Endothelial Dysfunction and Hypertension.Circulation research · 2024Article
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4 authors at 2 institutions in 1 country.
Funding
Abstract
Scientists have long established that fatty acids are the primary substrates for kidney mitochondria. However, to date we still do not know how long-chain and middle-chain fatty acids are oxidized at the mitochondrial level. Our previous research has shown that mitochondria from the heart, brain, and kidney oxidize palmitoylcarnitine at a high rate only in the presence of succinate, glutamate, or pyruvate. In this paper, we report properties of the isolated kidney mitochondria and how malate and succinate affect the oxidation of C16 and C8 acylcarnitines. The isolated kidney mitochondria contain very few endogenous substrates and require malate to oxidize pyruvate, glutamate, and C16 or C8 acylcarnitines. We discovered that with 10 µM of C16 or C8 acylcarnitines, low concentrations of malate (0.2 mM) or succinate (0.5 mM) enhance the States 4 and 3 respiratory rates several times. The highest respiration rates were observed with C16 or C8 acylcarnitines and 5 mM succinate mixtures. Results show that kidney mitochondria, unlike the heart and brain mitochondria, lack the intrinsic inhibition of succinate dehydrogenase. Additionally, results show that the oxidation of fatty acid by the small respirasome's supercomplex generates a high level of CoQH2, and this makes SDH in the presence of succinate reverse the flow of electrons from CoQH2 to reduce fumarate to succinate. Finally, we report evidence that succinate dehydrogenase is a key mitochondrial enzyme that allows fast oxidation of fatty acids and turns the TCA cycle function from the catabolic to the anabolic and anaplerotic metabolic pathways.
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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.