The regulation and turnover of mitochondrial uncoupling proteins
Open accessAbstract
Uncoupling proteins (UCP1, UCP2 and UCP3) are important in regulating cellular fuel metabolism and as attenuators of reactive oxygen species production through strong or mild uncoupling. The generic function and broad tissue distribution of the uncoupling protein family means that they are increasingly implicated in a range of pathophysiological processes including obesity, insulin resistance and diabetes mellitus, neurodegeneration, cardiovascular disease, immunity and cancer. The significant recent progress describing the turnover of novel uncoupling proteins, as well as current views on the physiological roles and regulation of UCPs, is outlined.
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Experimental evidence implicates fatty acids in the transport of protons by UCPs.
“It is unclear precisely how UCPs modulate proton leak; however, experimental evidence implicates fatty acids in the transport of protons by these inner mitochondrial membrane proteins (23).”
From Redox regulation of mitochondrial function (2012) · cites this paper as [23]
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References 122 · Cited by 146
- Authors
- Azzu, V., Jastroch, M., Divakaruni, A. S., & Brand, M. D.
- Affiliations
- MRC Mitochondrial Biology Unit (GB)
- Buck Institute for Research on Aging (US)
- Corresponding author
- Brand, Martin D.
- Venue
- Biochimica et Biophysica Acta (BBA) - Bioenergetics
- Publisher
- Elsevier BV
- Published
- 2010-06
- Volume
- 1797
- Issue
- 6-7
- Pages
- 785-791
- ISSN
- 0005-2728 (ISSN-L)
- PMC
- PMC2891119
- OpenAlex
- W2070728564
- Cited by
- 146
- References
- 122
- Citations by year
- 2026: 3 · 2025: 6 · 2024: 5 · 2023: 2 · 2022: 9 · 2021: 5 · 2020: 10 · 2019: 8 · 2018: 10 · 2017: 6 · 2016: 5 · 2015: 14 · 2014: 13 · 2013: 19 · 2012: 17
- FWCI
- 1.40
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Biochimica et Biophysica Acta (BBA) - Bioenergetics (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Site cant be reached (submittedVersion)
- Funders
- National Science Foundation
- Ellison Medical Foundation (AG-SS-2288-09, SS-2288-09)
- W. M. Keck Foundation
- Deutsche Forschungsgemeinschaft (JA 1884/2-1)
- National Institutes of Health (AG025708, AG025901)
- Medical Research Council
- National Institute on Aging (R01AG033542, PL1AG032118, P01AG025901, P30AG025708)
- National Institute of Dental and Craniofacial Research (UL1DE019608)
- 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 › ATP Synthase and ATPases Research
- Keywords
- uncoupling proteins, UCP1, UCP2, UCP3, mitochondrial uncoupling, protein turnover, protein regulation, reactive oxygen species, obesity, insulin resistance, diabetes mellitus, neurodegeneration, cardiovascular disease, immunity, cancer
- MeSH terms
- Uncoupling Protein 2, Uncoupling Protein 3, Uncoupling Protein 1, Animals, Diabetes Mellitus, Energy Metabolism, Humans, Insulin Resistance, Ion Channels, Mitochondria, Models, Biological, Obesity, Gene Expression, Mitochondrial Proteins
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