J. Lipid Res. Neurobiology of Lipids (ISSN1683-5506)
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A more recent version of this article appeared on December 1, 2006

Papers In Press, published online ahead of print September 27, 2006
J. Lipid Res., doi:10.1194/jlr.M600273-JLR200
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Submitted on June 22, 2006
Revised on September 27, 2006
Accepted on September 27, 2006

Trans geometric isomers of eicosapentaenoic acid lower LXRalpha -induced cellular triacylglycerol via suppression of sterol regulatory element binding protein-1c and peroxisome-proliferator-activated receptor-gamma co-activator 1beta

Nobuhiro Zaima, Tatsuya Sugawara, Dai Goto, and Takashi Hirata

Graduate School of Agriculture, kyoto university, kyoto city 606-8502

Corresponding Author: zaima{at}kais.kyoto-u.ac.jp

Dietary mono- or di-trans fatty acids with chain lengths of 18-22 significantly raise LDL cholesterol and lower HDL cholesterol in the plasma and is involved in a risk of cardiovascular diseases, but the effects of trans isomers of polyunsaturated fatty acids (PUFA) on lipid metabolism remain unknown. Dietary PUFA, especially eicosapentaenoic acid (EPA) in marine oils, improves serum lipid profiles by suppressing liver X receptor alpha (LXRa) activity in the liver. In the preset study, we compared the effects of trans geometrical isomers of EPA (TEPA) on triacylglycerol synthesis induced by a synthetic LXRa agonist (T0901317) with those of EPA in HepG2. TEPA significantly decreased the cellular triacylglycerol amount and the expression of mRNAs encoding fatty acid synthase, stearoyl CoA desaturase-1 and glycerol-3-phosphate acyltransferase induced by T0901317 than those in EPA treated cells. However, there was no significant difference between the suppressive effect of TEPA and EPA on sterol regulatory element binding protein-1c (SREBP-1c) expression. We found that TEPA, but not EPA, decreased the mRNA expression of peroxisome-proliferator-activated receptor-gamma co-activator 1beta(PGC-1b), LXRa and SREBP1 coactivator. These results suggest that the hypolipidemic effect of TEPA is attributed to decreased expression both of SREBP-1 and of PGC-1b.


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