ArticleFASEB bioAdvances2022
Membrane potential-dependent regulation of mitochondrial complex II by oxaloacetate in interscapular brown adipose tissue.
Article in FASEB bioAdvances, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 8 citations in OpenAlex.
- Cross-species urinary metabolomics identifies 2-hydroxyisovalerate as a candidate biomarker for mtDNA-based disorders.Metabolomics : Official journal of the Metabolomic Society · 2026Article
- Oxaloacetate inhibition of succinate dehydrogenase: mechanism and physiological implications.American journal of physiology. Cell physiology · 2026Review
- Sodium formate-induced mitochondrial impairment and cytotoxicity in neuronal cells reveal crucial pathogenic mechanisms underlying diabetic neuropathy and retinopathy.Scientific reports · 2025Article
- Complex II ambiguities-FADHThe Journal of biological chemistry · 2024Review
- Oxaloacetate regulates complex II respiration in brown fat: dependence on UCP1 expression.American journal of physiology. Cell physiology · 2023Article
- Metabolic clearance of oxaloacetate and mitochondrial complex II respiration: Divergent control in skeletal muscle and brown adipose tissue.Biochimica et biophysica acta. Bioenergetics · 2023Article
- Succinate Dehydrogenase, Succinate, and Superoxides: A Genetic, Epigenetic, Metabolic, Environmental Explosive Crossroad.Biomedicines · 2022Review
- Membrane potential-dependent regulation of mitochondrial complex II by oxaloacetate in interscapular brown adipose tissue.FASEB bioAdvances · 2022Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Classically, mitochondrial respiration responds to decreased membrane potential (ΔΨ) by increasing respiration. However, we found that for succinate-energized complex II respiration in skeletal muscle mitochondria (unencumbered by rotenone), low ΔΨ impairs respiration by a mechanism culminating in oxaloacetate (OAA) inhibition of succinate dehydrogenase (SDH). Here, we investigated whether this phenomenon extends to far different mitochondria of a tissue wherein ΔΨ is intrinsically low, i.e., interscapular brown adipose tissue (IBAT). Also, to advance our knowledge of the mechanism, we performed isotopomer studies of metabolite flux not done in our previous muscle studies. In additional novel work, we addressed possible ways ADP might affect the mechanism in IBAT mitochondria. UCP1 activity, and consequently ΔΨ, were perturbed both by GDP, a well-recognized potent inhibitor of UCP1 and by the chemical uncoupler carbonyl cyanide m-chlorophenyl hydrazone (FCCP). In succinate-energized mitochondria, GDP increased ΔΨ but also increased rather than decreased (as classically predicted under low ΔΨ) O
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