Decreased fatty acid synthesis due to mitochondrial uncoupling in adipose tissue
Language English Country United States Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
10973929
DOI
10.1096/fj.99-0965com
Knihovny.cz E-resources
- MeSH
- 3T3 Cells MeSH
- Energy Metabolism MeSH
- Gene Expression MeSH
- Ion Channels MeSH
- Fatty Acids biosynthesis MeSH
- Membrane Proteins metabolism MeSH
- Mitochondrial Proteins MeSH
- Mitochondria metabolism physiology MeSH
- Mice, Inbred C57BL MeSH
- Mice, Transgenic MeSH
- Mice MeSH
- Carrier Proteins metabolism MeSH
- Adipose Tissue cytology metabolism MeSH
- Uncoupling Protein 1 MeSH
- Animals MeSH
- Check Tag
- Male MeSH
- Mice MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Ion Channels MeSH
- Fatty Acids MeSH
- Membrane Proteins MeSH
- Mitochondrial Proteins MeSH
- Carrier Proteins MeSH
- Ucp1 protein, mouse MeSH Browser
- Uncoupling Protein 1 MeSH
Synthesis of fatty acid (FA) in adipose tissue requires cooperation of mitochondrial and cytoplasmic enzymes. Mitochondria are required for the production of ATP and they also support the formation of acetyl-CoA and NADPH in cytoplasm. Since cellular levels of all these metabolites depend on the efficiency of mitochondrial energy conversion, mitochondrial proton leak via uncoupling proteins (UCPs) could modulate FA synthesis. In 3T3-L1 adipocytes, 2,4-dinitrophenol depressed the synthesis of FA 4-fold while increasing FA oxidation 1. 5-fold and the production of lactate 14-fold. Inhibition of FA synthesis in 3T3-L1 adipocytes was proportional to the decrease in mitochondrial membrane potential. FA synthesis from D-[U-(14)C] glucose was reduced up to fourfold by ectopic UCP1 in the white fat of transgenic aP2-Ucp1 mice, reflecting the magnitude of UCP1 expression in different fat depots and the reduction of adiposity. Transcript levels for lipogenic enzymes were lower in the white fat of the transgenic mice than in the control animals. Our results show that uncoupling of oxidative phosphorylation depresses FA synthesis in white fat. Reduction of adiposity via mitochondrial uncoupling in white fat not only reflects increased energy expenditure, but also decreased in situ lipogenesis.
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