J. Lipid Res.
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A more recent version of this article appeared on April 1, 2004

Papers In Press, published online ahead of print January 16, 2004
J. Lipid Res., doi:10.1194/jlr.M300458-JLR200
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Submitted on November 3, 2003
Revised on December 19, 2003
Accepted on January 5, 2004

APOA5 gene variants, lipoprotein particle distribution and progression of coronary heart disease: results from the LOCAT study

Philippa J. Talmud, Steve Martin, Marja-Riitta Taskinen, M. Heikki Frick, Markku S. Nieminen, Y. Antero Kesäniemi, Amos Pasternack, Steve E. Humphries, and Mikko Syvänne

Department of Medicine, University College London, London, London WC1E 6JF

Corresponding Author: p.talmud{at}ucl.ac.uk

Animal and human studies support a role for apoAV in triglyceride (TG) metabolism. We examined the relationship of APOA5 -1131T>C and S19W with lipid subfractions and progression of atherosclerosis in the LOCAT gemfibrozil study of post by-pass men. Compared to –1131TT men (n=242) , carriers of the –1131C allele (n=54) had significantly higher total TG (p=0.03), reflected in significantly increased very low density lipoprotein (VLDL) mass (higher VLDL-TG, VLDL-cholesterol, VLDL-protein and surface lipids (all p<0.05)). Since apoB levels were unaffected by genotype this suggests an increase in VLDL size and not number. Compared to the 19SS men (n=268), 19W carriers (n=44) had higher intermediate density lipoprotein (IDL)-TG, IDL-cholesterol (p=0.04) and IDL-surface components (free cholesterol (p=0.005) and phospholipids (p=0.017)), but not protein content, suggesting an increase in IDL lipid-enrichment resulting in an increase in IDL size. 19W carriers also showed a trend towards increased progression of atherogenesis; change in average diameter of segments (-0.46 (+ 0.011 mm) compared to –0.016 (+0.006mm) in 19SS men (p=0.08). There was no effect of genotype on the response of these parameters to gemfibrozil treatment. These results shed new light on the role of APOA5 variants in TG metabolism and CHD risk.


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