Physiological diversity of mitochondrial oxidative phosphorylation
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To investigate the physiological diversity in the regulation and control of mitochondrial oxidative phosphorylation, we determined the composition and functional features of the respiratory chain in muscle, heart, liver, kidney, and brain. First, we observed important variations in mitochondrial content and infrastructure via electron micrographs of the different tissue sections. Analyses of respiratory chain enzyme content by Western blot also showed large differences between tissues, in good correlation with the expression level of mitochondrial transcription factor A and the activity of citrate synthase. On the isolated mitochondria, we observed a conserved molar ratio between the respiratory chain complexes and a variable stoichiometry for coenzyme Q and cytochrome c, with typical values of [1-1.5]:[30-135]:[3]:[9-35]:[6.5-7.5] for complex II:coenzyme Q:complex III:cytochrome c:complex IV in the different tissues. The functional analysis revealed important differences in maximal velocities of respiratory chain complexes, with higher values in heart. However, calculation of the catalytic constants showed that brain contained the more active enzyme complexes. Hence, our study demonstrates that, in tissues, oxidative phosphorylation capacity is highly variable and diverse, as determined by different combinations of 1) the mitochondrial content, 2) the amount of respiratory chain complexes, and 3) their intrinsic activity. In all tissues, there was a large excess of enzyme capacity and intermediate substrate concentration, compared with what is required for state 3 respiration. To conclude, we submitted our data to a principal component analysis that revealed three groups of tissues: muscle and heart, brain, and liver and kidney.
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Protein expression of multiple OXPHOS components and Tfam (expressed per milligram of protein) and citrate synthase activity are also lower in liver (e.g., 7% that of cardiac muscle).
“Protein expression of multiple OXPHOS components and Tfam (expressed per milligram of protein) and citrate synthase activity are also lower in liver (e.g., 7% that of cardiac muscle) (211).”
From The role of mitochondria in the pathogenesis of type 2 diabetes (2010) · cites this paper as [211]
Isolated hepatic mitochondria have relative reductions in OXPHOS proteins, respiratory chain cytochromes, and maximal activity of complexes III and IV.
“Functionally, isolated hepatic mitochondria have relative reductions in OXPHOS proteins, respiratory chain cytochromes, and maximal activity of complexes III and IV (211).”
From The role of mitochondria in the pathogenesis of type 2 diabetes (2010) · cites this paper as [211]
Despite lower OXPHOS capacity, state 3 respiration and respiratory control ratio are equivalent in liver and muscle, indicating differences in relative substrate concentrations and lower 'excess capacity' in liver.
“Despite lower OXPHOS capacity, state 3 respiration and respiratory control ratio are equivalent in liver and muscle, indicating differences in relative substrate concentrations and lower”
From The role of mitochondria in the pathogenesis of type 2 diabetes (2010) · cites this paper as [211]
Fatty acid-induced reductions in insulin receptor number and function in the liver may also reduce hepatic insulin clearance, causing systemic hyperinsulinemia, itself a contributor to both insulin resistance and reduced mitochondrial function.
“Fatty acid-induced reductions in insulin receptor number and function in the liver (211) may also reduce hepatic insulin clearance (226), causing systemic hyperinsulinemia, itself a contributor to both insulin resistance and reduced mitochondrial function (214,227,228).”
From The role of mitochondria in the pathogenesis of type 2 diabetes (2010) · cites this paper as [211]
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References 52 · Cited by 297
- Authors
- Benard, G., Faustin, B., Passerieux, E., Galinier, A., Rocher, C., Bellance, N., Delage, J.-P., Casteilla, L., Letellier, T., & Rossignol, R.
- Affiliations
- Inserm (FR)
- Venue
- American Journal of Physiology-Cell Physiology
- Publisher
- American Physiological Society
- Published
- 2006-12
- Volume
- 291
- Issue
- 6
- Pages
- C1172-C1182
- ISSN
- 0363-6143 (ISSN-L)
- 1522-1563
- OpenAlex
- W2123462780
- Cited by
- 297
- References
- 52
- Citations by year
- 2026: 10 · 2025: 8 · 2024: 9 · 2023: 16 · 2022: 8 · 2021: 21 · 2020: 8 · 2019: 19 · 2018: 15 · 2017: 9 · 2016: 11 · 2015: 9 · 2014: 20 · 2013: 19 · 2012: 33
- FWCI
- 6.11
- Type
- journal article
- Language
- en
- Open access
- green
- hal.umontpellier.fr
- Licence
- other-oa
- Locations
- American Journal of Physiology-Cell Physiology (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion, other-oa)
- Funders
- Institut National de la Santé et de la Recherche Médicale
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Coenzyme Q10 studies and effects
- Keywords
- mitochondrial oxidative phosphorylation, electron transport chain, tissue differences, coenzyme Q10, cytochrome c, cytochrome c oxidase, cytochrome bc1 complex, complex II, mitochondrial content, TFAM, citrate synthase, state 3 respiration, heart, brain, liver, kidney, muscle
- MeSH terms
- Animals, Brain, Citrate (si)-Synthase, Electron Transport Complex IV, Cytochromes, Electron Transport, Humans, Kidney, Liver, Male, Mitochondria, Muscles, Myocardium, Oxidative Phosphorylation, Electron Transport Complex III, Rats, Wistar, Mitochondrial Proteins, Electron Transport Complex II, Electron Transport Complex I, Rats
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