Current smokers with hyperlipidemia lack elevated preβ1-high-density lipoprotein concentrations.

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.