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1Department of Adipose Tissue Biology, Institute of Physiology, Academy of Sciences of the Czech Republic, Prague, Czech Republic
1Correspondence: Institute of Physiology, Academy of Sciences of the Czech Republic, Vide
ská 1083, CZ - 142 20 Prague, Czech Republic. E-mail: kopecky{at}biomed.cas.cz
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-14C] 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.—Rossmeisl, M., Syrov
, I.,
Baumruk, F., Flachs, P., Janovská, P., Kopeck, J.
Decreased fatty acid synthesis due to mitochondrial uncoupling in
adipose tissue.
Key Words: UCP • lipogenesis • C57BL/6J mice • 3T3-L1 • obesity
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