LAUSR

BACKGROUND Preβ1-high-density lipoprotein (HDL) is an efficient acceptor of cell-derived free cholesterol, which is converted into lipid-rich HDL by lecithin-cholesterol acyltransferase. Previous studies have shown that preβ1-HDL is significantly higher in individuals with hyperlipidemia. Preβ1-HDL concentrations may be altered in smokers, who are at high risk for atherosclerosis. OBJECTIVE The aim of the present study was to investigate the effect of smoking on preβ1-HDL concentrations. METHODS We measured the preβ1-HDL concentration and lecithin-cholesterol acyltransferase-dependent conversion rate (CHTpreβ1) in 74 men (39 nonsmokers and 35 smokers) using an immunoassay. RESULTS The smoker and nonsmoker groups were further divided into normolipidemic and hyperlipidemic subjects. Among nonsmokers, the mean preβ1-HDL concentration was 27% higher in hyperlipidemics than in normolipidemics (25.5 ± 6.7 vs 20.3 ± 4.6 mg/L apoAI, P < .01). In contrast, mean preβ1-HDL concentrations did not differ between hyperlipidemic and normolipidemic smokers (19.9 ± 3.1 vs 22.4 ± 6.9 mg/L apoAI). We found a positive correlation between preβ1-HDL concentration and CHTpreβ1 in nonsmokers, but not in smokers. Smoking a single cigarette did not change preβ1-HDL concentrations or CHTpreβ1. Compared with nonsmokers, preβ1-HDL concentrations were relatively low in hyperlipidemic smokers but not in normolipidemic smokers, and CHTpreβ1 was not a significant determinant of preβ1-HDL concentrations in smokers. CONCLUSION Our findings suggest that smoking may be disadvantageous to individuals with hyperlipidemia because preβ1-HDL metabolism is altered.