HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Mero, N. Articles by Taskinen, M-R. Search for Related Content PubMed PubMed Citation Articles by Mero, N. Articles by Taskinen, M-R. Social Bookmarking                      What's this?

The Journal of Lipid Research, Vol. 39, 1493-1502, July 1998
Copyright © 1998 by Lipid Research, Inc.

Original Article

Decreased postprandial high density lipoprotein cholesterol and apolipoproteins A-I and E in normolipidemic smoking men: relations with lipid transfer proteins and LCAT activities

Correspondence to: M-R. Taskinen.

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.—Mero, N., A. Van Tol, L. M. Scheek, T. Van Gent, C. Labeur, M. Rosseneu, and M-R. Taskinen. Decreased postprandial high density lipoprotein cholesterol and apolipoproteins A-I and E in normolipidemic smoking men: relationship with lipid transfer proteins and LCAT activities. J. Lipid Res. 1998. 39: 1493–1502.

Supplementary key words: alimentary lipemia, atherogenesis, triglyceride-rich lipoproteins, apolipoprotein C, apolipoprotein A-I particles, cholesteryl ester transfer protein, phospholipid transfer protein, esterification rate

CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

This article has been cited by other articles:

				M. D. Ashen and R. S. Blumenthal Low HDL Cholesterol Levels N. Engl. J. Med., September 22, 2005; 353(12): 1252 - 1260. [Full Text] [PDF]

				D. J Freeman, N. J Samani, V. Wilson, A. D McMahon, P. S Braund, S. Cheng, M. J Caslake, C. J Packard, D. Gaffney, and on behalf of the West of Scotland Study Group A polymorphism of the cholesteryl ester transfer protein gene predicts cardiovascular events in non-smokers in the West of Scotland Coronary Prevention Study Eur. Heart J., October 2, 2003; 24(20): 1833 - 1842. [Abstract] [Full Text] [PDF]

				T. Kujiraoka, M. N. Nanjee, T. Oka, M. Ito, M. Nagano, C. J. Cooke, S. Takahashi, W. L. Olszewski, J. S. Wong, I. P. Stepanova, et al. Effects of Intravenous Apolipoprotein A-I/Phosphatidylcholine Discs on LCAT, PLTP, and CETP in Plasma and Peripheral Lymph in Humans Arterioscler. Thromb. Vasc. Biol., September 1, 2003; 23(9): 1653 - 1659. [Abstract] [Full Text] [PDF]

				H. M. Colhoun, M.-R. Taskinen, J. D. Otvos, P. van den Berg, J. O'Connor, and A. Van Tol Relationship of Phospholipid Transfer Protein Activity to HDL and Apolipoprotein B-Containing Lipoproteins in Subjects With and Without Type 1 Diabetes Diabetes, November 1, 2002; 51(11): 3300 - 3305. [Abstract] [Full Text] [PDF]

				M. Guerin, P. Egger, C. Soudant, W. Le Goff, A. van Tol, R. Dupuis, and M. J. Chapman Cholesteryl ester flux from HDL to VLDL-1 is preferentially enhanced in type IIB hyperlipidemia in the postprandial state J. Lipid Res., October 1, 2002; 43(10): 1652 - 1660. [Abstract] [Full Text] [PDF]

				S. J. Murdoch, M. C. Carr, H. Kennedy, J. D. Brunzell, and J. J. Albers Selective and independent associations of phospholipid transfer protein and hepatic lipase with the LDL subfraction distribution J. Lipid Res., August 1, 2002; 43(8): 1256 - 1263. [Abstract] [Full Text] [PDF]

				S. J. Murdoch, M. C. Carr, J. E. Hokanson, J. D. Brunzell, and J. J. Albers PLTP activity in premenopausal women: relationship with lipoprotein lipase, HDL, LDL, body fat, and insulin resistance J. Lipid Res., February 1, 2000; 41(2): 237 - 244. [Abstract] [Full Text]

				S. C. Riemens, A. Van Tol, W. J. Sluiter, and R. P. F. Dullaart Acute and chronic effects of a 24-hour intravenous triglyceride emulsion challenge on plasma lecithin: cholesterol acyltransferase, phospholipid transfer protein, and cholesteryl ester transfer protein activities J. Lipid Res., August 1, 1999; 40(8): 1459 - 1466. [Abstract] [Full Text]