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Journal of Lipid Research, Vol 32, 1457-1463, Copyright © 1991 by Lipid Research, Inc.
EZ Amri, G Ailhaud and P Grimaldi
Fatty acids behave as activators of the aP2 gene expression in committed,
lipid-free, non-terminally differentiated Ob1771 cells. Like fatty acids,
dexamethasone provokes a dose-dependent accumulation of aP2 mRNA. However,
fatty acids and dexamethasone act through different mechanisms to activate
the aP2 gene expression since i) fatty acids and dexamethasone act in a
synergistic manner; ii) the effect of dexamethasone is rapid and transient
(maximal effect after 8 h), whereas that of fatty acids is slower, and
maintained as long as the inducer is present and is fully reversible upon
fatty acid removal; iii) the induction of the aP2 gene expression by
dexamethasone does not require ongoing protein synthesis, while the
response to fatty acids is completely prevented by cycloheximide; and iv)
the induction of the aP2 gene expression by fatty acids but not by
dexamethasone is confined to preadipocyte cell lines. This suggests that
the process of activation by fatty acids, rather than the expression of the
aP2 gene, is unique to adipose cells. Besides their effects on the aP2
gene, fatty acids activate the expression of the acyl CoA synthetase gene
which encodes another protein involved in fatty acid metabolism. Activation
of both genes by fatty acids appears not to be mediated by the CCAAT
enhancer binding protein, a nuclear factor reported as transactivator of
the aP2 promoter activity, since the enhancer binding protein mRNA is not
expressed under these conditions.
ARTICLES
Regulation of adipose cell differentiation. II. Kinetics of induction of the aP2 gene by fatty acids and modulation by dexamethasone
Centre de Biochimie (CNRS-UMR 134), U.F.R. Sciences, Universite de Nice- Sophia Antipolis, France.
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