Decreased postprandial high density lipoprotein cholesterol and apolipoproteins A-I and E in normolipidemic smoking men: relations with lipid transfer proteins and LCAT activities.
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.
Department of Medicine, Helsinki University Central Hospital, Finland.
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Mero
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Van Tol
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LM
Scheek
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Van Gent
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Labeur
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Rosseneu
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MR
Taskinen
D000328:Adult; D016632:Apolipoprotein A-I / Q000097:blood*; D001057:Apolipoproteins E / Q000097:blood*; D001786:Blood Glucose / Q000032:analysis; D002096:C-Peptide / Q000097:blood; D002352:Carrier Proteins / Q000097:blood*; D002784:Cholesterol / Q000097:blood*; D053480:Cholesterol Ester Transfer Proteins; D002788:Cholesterol Esters / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood*; D004041:Dietary Fats; D006023:Glycoproteins; D006801:Humans; D007328:Insulin / Q000097:blood; D008079:Lipoproteins, VLDL / Q000097:blood; D008297:Male; D007862:Phosphatidylcholine-Sterol O-Acyltransferase / Q000097:blood*; D019518:Postprandial Period; D012016:Reference Values; D012907:Smoking / Q000097:blood*; D013997:Time Factors
D016632:Apolipoprotein A-I; D001057:Apolipoproteins E; D001786:Blood Glucose; D002096:C-Peptide; C506642:CETP protein, human; D002352:Carrier Proteins; D053480:Cholesterol Ester Transfer Proteins; D002788:Cholesterol Esters; D008076:Cholesterol, HDL; D004041:Dietary Fats; D006023:Glycoproteins; D007328:Insulin; D008079:Lipoproteins, VLDL; D002784:Cholesterol; D007862:Phosphatidylcholine-Sterol O-Acyltransferase