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J. Lipid Res.
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A more recent version of this article appeared on October 1, 2003

Papers In Press, published online ahead of print July 16, 2003
J. Lipid Res., doi:10.1194/jlr.M300118-JLR200
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Submitted on March 14, 2003
Revised on July 9, 2003
Accepted on July 16, 2003

The T111I missense mutation of the endothelial lipase gene modulates the relationship between dietary fat intake and the HDL profile in women

Marie-Eve Paradis, Patrick Couture, Yohan Bossé, Jean-Pierre Després, Louis Pérusse, Claude Bouchard, Marie-Claude Vohl, and Benoît Lamarche

INAF, Nutraceuticals and Functional Foods Institute, Québec, Québec G1K 7P4

Corresponding Author: benoit.lamarche{at}inaf.ulaval.ca

Endothelial lipase (EL) has recently been added to the intravascular lipase gene superfamily. Unlike lipoprotein lipase and hepatic lipase, EL has been reported to be almost exclusively a phospholipase, with particular affinity for high-density lipoproteins (HDL). We sought to examine the impact of the T111I missense mutation in exon 3 of the EL gene on the lipoprotein-lipid profile of subjects from the Québec Family Study and its potential interaction effect with dietary fat. The study sample included 281 women and 216 men aged between 17 and 76 years. Plasma HDL3-C levels of I111I homozygotes women were higher compared with women carrying the wild type allele (T111T: 0.71 ± 0.15, T111I: 0.70 ± 0.15, I111I: 0.77 ± 0.17 mmol/L, P=0.03). These differences were not attenuated when adjusted for body mass index and visceral adipose tissue levels and were not observed among men. Dietary polyunsaturated fatty acids (PUFA) interacted with the T111I mutation to modulate apoA-I and HDL3-C levels among women. Specifically, our data showed that a diet rich in PUFA (>4.2% of energy), was associated with increased plasma apoA-I levels among women carriers of the I111 allele and with decreased plasma apoA-I among women bearing both wild-type alleles (P=0.002). A similar interaction was observed with plasma HDL3-C levels (P=0.003). These interactions were not observed among men. This study demonstrated that the EL T111I mutation appears to have modest effect on plasma HDL levels. However, the observation of a gene-diet interaction effects among women suggest that the T111I missense mutation may confer protection against the lowering effect of a high dietary PUFA intake on plasma apoA-I and HDL3-C levels.


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