Stronger control of ATP/ADP by proton leak in pancreatic β-cells than skeletal muscle mitochondria
Open accessAbstract
Pancreatic beta cells respond to rising blood glucose concentrations by increasing their oxidative metabolism, which leads to an increased ATP/ADP ratio, closure of KATP channels, depolarization of the plasma membrane potential, influx of calcium and the eventual secretion of insulin. Such a signalling mechanism implies that the ATP/ADP ratio is flexible in beta cells (β-cells), which is in contrast with other cell types (e.g. muscle and liver) that maintain a stable ATP/ADP poise while respiring at widely varying rates. To determine whether this difference in flexibility is accounted for by mitochondrial peculiarities, we performed a top-down metabolic control analysis to quantitatively assess how ATP/ADP is controlled in mitochondria isolated from rat skeletal muscle and cultured beta cells. We show that the ATP/ADP ratio is more strongly controlled (approx. 7.5-fold) by proton leak in beta cells than in muscle. The comparatively high importance of proton leak in beta cell mitochondria (relative to phosphorylation) is evidenced furthermore by its relatively high level of control over membrane potential and overall respiratory activity. Modular-kinetic analysis of oxidative phosphorylation reveals that these control differences can be fully explained by a higher relative leak activity in beta cell mitochondria, which results in a comparatively high contribution of proton leak to the overall respiratory activity in this system.
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ATP/ADP ratio is more regulated by mitochondria in islet β cells than in skeletal muscle.
“Interestingly, a kinetic analysis (9) revealed that the ATP/ADP ratio was much more regulated by mitochondria in islet β cells (modeled by INS-1E insulinoma cells) than by mitochondria of skeletal muscle, supporting the importance of mitochondria in regulating islet insulin secretion.”
From Mitochondrial Dysfunction in Diabetes: From Molecular Mechanisms to Functional Significance and Therapeutic Opportunities (2010) · cites this paper as [9]
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- Authors
- Affourtit, C., & Brand, M. D.
- Affiliations
- MRC Mitochondrial Biology Unit (GB)
- Venue
- Biochemical Journal
- Publisher
- Portland Press Ltd.
- Published
- 2005-12-12
- Volume
- 393
- Issue
- 1
- Pages
- 151-159
- ISSN
- 0264-6021 (ISSN-L)
- 1470-8728
- PMC
- PMC1383673
- OpenAlex
- W2028086207
- Cited by
- 71
- References
- 52
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 8 · 2023: 1 · 2022: 3 · 2021: 2 · 2020: 2 · 2019: 1 · 2018: 3 · 2017: 2 · 2016: 5 · 2015: 3 · 2014: 4 · 2013: 6 · 2012: 3
- FWCI
- 1.00
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Biochemical Journal (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Medical Research Council
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › ATP Synthase and ATPases Research
- Keywords
- ATP/ADP ratio, mitochondrial proton leak, pancreatic beta cells, skeletal muscle mitochondria, metabolic control analysis, oxidative phosphorylation, mitochondrial membrane potential, mitochondrial respiration, insulin secretion, glucose-stimulated insulin secretion
- MeSH terms
- Adenosine Diphosphate, Adenosine Triphosphate, Animals, Cell Membrane, Female, Membrane Potentials, Mitochondria, Oxygen Consumption, Protons, Rats, Wistar, Muscle, Skeletal, Insulin-Secreting Cells, Rats
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