Genetic and physiologic analysis of the role of uncoupling protein 3 in human energy homeostasis.
Open accessAbstract
By virtue of its potential effects on rates of energy expenditure, uncoupling protein 3 (UCP3) is an obesity candidate gene. We identified nine sequence variants in UCP3, including Val9Met, Val102Ile, Arg282Cys, and a splice site mutation in the intron between exons 6 and 7. The splice mutation results in an inability to synthesize mRNA for the long isoform (UCP3L) of UCP3. Linkage (sib pair), association, and transmission disequilibrium testing studies on 942 African-Americans did not suggest a significant effect of UCP3 on body composition in this group. In vastus lateralis skeletal muscle of individuals homozygous for the splice mutation, no UCP3L mRNA was detectable; the short isoform (UCP3S) was present in an increased amount. In this muscle, we detected no alterations of in vitro mitochondrial coupling activity, mitochondrial respiratory enzyme activity, or systemic oxygen consumption or respiratory quotient at rest or during exercise. These genetic and physiologic data suggest the following possibilities: UCP3S has uncoupling capabilities equivalent to UCP3L; other UCPs may compensate for a deficiency of bioactive UCP3L; UCP3L does not function primarily as a mitochondrial uncoupling protein.
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Skeletal muscle mitochondria from a human with dysfunctional UCP3 showed no change in respiratory coupling.
“In addition, skeletal muscle mitochondria from a human with dysfunctional UCP3 showed no change in respiratory coupling (62).”
From Mitochondrial Dysfunction in Diabetes: From Molecular Mechanisms to Functional Significance and Therapeutic Opportunities (2010) · cites this paper as [62]
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- Authors
- Chung, W. K., Luke, A., Cooper, R. S., Rotini, C., Vidal-Puig, A., Rosenbaum, M., Chua, M., Solanes, G., Zheng, M., Zhao, L., LeDuc, C., Eisberg, A., Chu, F., Murphy, E., Schreier, M., Aronne, L., Caprio, S., Kahle, B., Gordon, D., Leal, S. M., Goldsmith, R., Andreu, A. L., Bruno, C., DiMauro, S., & Leibel, R. L.
- Affiliations
- Columbia University Irving Medical Center (US)
- Department of Pediatrics and Medicine, Naomi Berrie Diabetes Center, Columbia University College of Physicians and Surgeons, New York, New York, USA.
- ORCID
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 1999-09-01
- Volume
- 48
- Issue
- 9
- Pages
- 1890-1895
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- PMC
- PMC6155469
- OpenAlex
- W2102547070
- Cited by
- 48
- References
- 31
- Citations by year
- 2022: 1 · 2015: 1 · 2013: 1
- FWCI
- 2.53
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Diabetes (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Civil War Book Review (submittedVersion)
- Funders
- National Institutes of Health (5r01dk030583-18)
- National Heart, Lung, and Blood Institute (R01HL053353)
- National Human Genome Research Institute (R01HG000008)
- National Institute of Diabetes and Digestive and Kidney Diseases (T32 DK07559, R01DK052431, DK-30583, R01DK053477, R37DK053477, P30DK026687, T32DK007559, DK-52431)
- 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 › Genetics › Genetic Associations and Epidemiology
- Keywords
- UCP3, obesity, energy homeostasis, energy expenditure, splice site mutation, mitochondrial uncoupling, body composition, African Americans, genetic variants, mitochondrial respiratory enzymes, oxygen consumption, respiratory quotient
- MeSH terms
- Uncoupling Protein 3, Black or African American, Carrier Proteins, Energy Metabolism, Hispanic or Latino, Homeostasis, Humans, Ion Channels, Genetic Linkage, Mitochondria, Linkage Disequilibrium, Alternative Splicing, Mitochondrial Proteins, Black People, White People, Asian People
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