7f8aa479-4638-48cb-b473-c6bdc51aabac
title
APOA5  gene variants, lipoprotein particle distribution, and progression of coronary heart disease: results from the LOCAT study.
acd21656-6eda-4ca0-8c73-9338f5e1928a
abstract
Animal and human studies support a role for  apolipoprotein A-V (apoA-V)  in triglyceride (TG) metabolism. We examined the relationship of  APOA5   -1131T>C  and  S19W  with lipid subfractions and progression of atherosclerosis in the Lopid Coronary Angiography Trial. Compared with  -1131TT  men (n = 242), carriers of the  -1131C  allele (n = 54) had significantly higher total TG (P = 0.03), reflected in significantly increased VLDL mass [higher VLDL-TG, VLDL-cholesterol, VLDL-protein, and surface lipids (all P < 0.05)]. Because  apoB  levels were unaffected by genotype, this suggests an increase in VLDL size and not number. Compared with  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 toward increased progression of atherogenesis, as measured by change in average diameter of segments (-0.46 +/- 0.011 mm compared with -0.016 +/- 0.006 mm) 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 coronary heart disease risk.