HDL biology
Smoking lowers CETP activity and worsens postprandial HDL loss in normolipidemic men (J Lipid Res 1998)
Original title: Decreased postprandial high density lipoprotein cholesterol and apolipoproteins A-I and E in normolipidemic smoking men: relations with lipid transfer proteins and LCAT activities
Twelve male smokers and 12 non-smokers with comparable fasting lipoprotein profiles, BMI, and age underwent fasting and postprandial lipoprotein analysis to test whether smoking affects HDL composition and lipid transfer protein activities after a mixed meal. Postprandial apoA-I, LpA-I, HDL-cholesterol, and HDL apoE concentrations decreased in smokers but stayed unchanged in controls, while cholesterol and apoE rose significantly in the triglyceride-rich lipoprotein fraction in smokers. Fasting LCAT and PLTP activities and esterification and phospholipid transfer rates were comparable between groups, but fasting CETP activity was lower in smokers, and postprandially CETP and PLTP activities decreased in smokers relative to controls even as esterification rate increased. The authors conclude that healthy smokers show altered postprandial HDL composition and lipid transfer protein activity, potentially indicating impaired reverse cholesterol transport that promotes atherogenesis.
Original abstract
We have previously reported that normolipidemic smokers are lipid intolerant due to increased responses of triglyceride-rich lipoproteins (TRL) apolipoprotein B-48, triglyceride (TG), and retinyl esters to a mixed meal compared to non-smokers. To investigate whether postprandial high density lipoprotein (HDL), apolipoprotein A-I (apoA-I), apolipoprotein A-II (apoA-II), and apolipoprotein E (apoE) concentrations or lipid transfer protein activities are affected by cigarette smoking, we investigated 12 male smokers and 12 non-smokers with comparable fasting lipoprotein profile, BMI, and age. Plasma samples obtained after an overnight fast and postprandially were separated by density gradient ultracentrifugation. Postprandial apoA-I, lipoprotein AI-particles (LpA-I), HDL-cholesterol, and HDL apoE concentrations decreased in smokers, but remained unchanged in controls. Concomitantly, cholesterol and apoE concentrations increased significantly in TRL fractions in smokers. Fasting lecithin:cholesterol acyltransferase (LCAT) and phospholipid transfer protein (PLTP) activity levels, as well as esterification rates (EST) and phospholipid transfer rates were comparable between the groups. Cholesteryl ester transfer protein (CETP) activity levels were lower in the smokers. Postprandially EST increased, but CETP and PLTP activities deceased in smokers as compared to controls. We conclude, that even healthy, normolipidemic smokers have altered postprandial high density lipoprotein (HDL) cholesterol and apolipoprotein composition, as well as lipid transfer protein activities. The shift of cholesterol and apoE from HDL to the triglyceride-rich lipoprotein (TRL) fraction, together with decreased plasma apoA-I and LpA-I concentrations during alimentary lipemia may indicate impaired reverse cholesterol transport. Both the postprandial increase in TRL and the lowering of HDL may promote atherogenesis in smokers.
Summary written by cetpinhibition.org from the published abstract; figures as published. Page updated 19 August 2026. Methods.