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A more recent version of this article appeared on September 1, 2006
Papers In Press, published online ahead of print June 12, 2006
J. Lipid Res., doi:10.1194/jlr.M600233-JLR200
Submitted on May 31, 2006
Accepted on June 11, 2006
Apolipoprotein av, triglycerides and risk of future coronary artery disease in apparently healthy men and women; the prospective epic-norfolk population study
Stefan F.C. Vaessen, Frank G. Schaap, Jan Albert Kuivenhoven, Albert K. Groen, Barbara A. Hutten, S. Matthijs Boekholdt, Hiroaki Hattori, Manjinder S. Sandhu, Sheila A. Bingham, Robert Luben, Jutta A. Palmen, Nicholas J. Wareham, Steve E. Humphries, John J. P. Kastelein, Phillipa J. Talmud, and Kay-Tee Khaw
Dept. Vascular Medicine, Academic Medical Center, Amsterdam 1105 AZ
Corresponding Author: s.f.vaessen{at}amc.uva.nl
In mouse models apolipoprotein (apo) AV exhibits triglyceride-lowering effects. We investigated the apoAV: triglyceride relationship and the association of apoAV with coronary artery disease (CAD) risk by determining serum apoAV levels and genotypes in a nested case (n=1034): control (n=2031) study. In both univariate and multivariate analysis, apoAV levels showed no association with future CAD (p=0.4 and p=0.5, respectively). Unexpectedly there was a significant positive correlation between serum apoAV and TG, in men and women (r=0.36 and 0.28, respectively, p<0.001 each), but a negative correlation between apoAV and LPL mass (r=-0.14 and -0.12, for men and women respectively, p<0.001 each). The frequency of the c.56C>G polymorphism did not differ between cases and controls despite significant positive association of c.56G with both apoAV and TG levels. For 1131T>C, the minor allele was significantly associated with lower apoAV yet higher TG levels, and was overrepresented in cases (p=0.047). The association of 1131T>C with CAD risk was, however, independent of apoAV levels and likely acts through linkage disequilibrium with APOC3 variants. The positive correlation of apoAV levels with TG levels, negative correlation with LPL levels and lack of association with CAD risk highlights the need for further human studies to clarify the role of apoAV.

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