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) All Versions of this Article: M400480-JLR200v1 46/8/1643    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Söderlund, S. Articles by Taskinen, M.-R. Search for Related Content PubMed PubMed Citation Articles by Söderlund, S. Articles by Taskinen, M.-R. Social Bookmarking                      What's this?

Journal of Lipid Research, Vol. 46, 1643-1651, August 2005
Copyright © 2005 by American Society for Biochemistry and Molecular Biology

Hypertriglyceridemia is associated with preß-HDL concentrations in subjects with familial low HDL

Sanni Söderlund^*, Aino Soro-Paavonen^*, Christian Ehnholm, Matti Jauhiainen and Marja-Riitta Taskinen^1,*

^* Division of Cardiology, Department of Medicine, University of Helsinki, Helsinki, Finland
Department of Molecular Medicine, Biomedicum, National Public Health Institute, Helsinki, Finland

Published, JLR Papers in Press, May 16, 2005. DOI 10.1194/jlr.M400480-JLR200

¹ To whom correspondence should be addressed. e-mail: marja-riitta.taskinen{at}helsinki.fi

Preß-HDL particles act as the primary acceptors of cellular cholesterol in reverse cholesterol transport (RCT). An impairment of RCT may be the reason for the increased risk of coronary heart disease (CHD) in subjects with familial low HDL. We studied the levels of serum preß-HDL and the major regulating factors of HDL metabolism in 67 subjects with familial low HDL and in 64 normolipidemic subjects. We report that the subjects with familial low HDL had markedly reduced preß-HDL concentrations compared with the normolipidemic subjects (17.4 ± 7.2 vs. 23.4 ± 7.8 mg apolipoprotein A-I/dl; P < 0.001). A positive correlation was observed between preß-HDL concentration and serum triglyceride (TG) level (r = 0.334, P = 0.006). In addition, serum TG level was found to be the strongest predictor of preß-HDL concentration in subjects with familial low HDL. The activities of cholesteryl ester transfer protein and hepatic lipase were markedly increased in subjects with familial low HDL without a significant correlation to preß-HDL concentration.

Our results support the hypothesis that impaired RCT is one mechanism behind the increased risk for CHD in subjects with familial low HDL.

Abbreviations: apoA-I, apolipoprotein A-I; BMI, body mass index; CETP, cholesteryl ester transfer protein; CHD, coronary heart disease; FC, free cholesterol; HDL-C, high density lipoprotein-cholesterol; HOMA IR, homeostasis model assessment for insulin resistance; LpA-I, lipoprotein A-I; LpA-I/A-II, lipoprotein A-I/A-II; PLTP, phospholipid transfer protein; RCT, reverse cholesterol transport; TC, total cholesterol; TG, triglyceride; W/H ratio, waist/hip ratio

Supplementary key words reverse cholesterol transport • coronary heart disease • hepatic lipase • phospholipid transfer protein • cholesteryl ester transfer protein • insulin resistance • metabolic syndrome • apolipoprotein A-I • high density lipoprotein

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

This article has been cited by other articles:

				E. K. Young, C. Chatterjee, and D. L. Sparks HDL-ApoE Content Regulates the Displacement of Hepatic Lipase from Cell Surface Proteoglycans Am. J. Pathol., July 1, 2009; 175(1): 448 - 457. [Abstract] [Full Text] [PDF]

				S. Nakanishi, R. Vikstedt, S. Soderlund, M. Lee-Rueckert, A. Hiukka, C. Ehnholm, M. Muilu, J. Metso, J. Naukkarinen, L. Palotie, et al. Serum, but not monocyte macrophage foam cells derived from low HDL-C subjects, displays reduced cholesterol efflux capacity J. Lipid Res., February 1, 2009; 50(2): 183 - 192. [Abstract] [Full Text] [PDF]

				C. Wolfrum, J. J. Howell, E. Ndungo, and M. Stoffel Foxa2 Activity Increases Plasma High Density Lipoprotein Levels by Regulating Apolipoprotein M J. Biol. Chem., June 13, 2008; 283(24): 16940 - 16949. [Abstract] [Full Text] [PDF]

				A. Soro-Paavonen, J. Naukkarinen, M. Lee-Rueckert, H. Watanabe, E. Rantala, S. Soderlund, A. Hiukka, P. T. Kovanen, M. Jauhiainen, L. Peltonen, et al. Common ABCA1 variants, HDL levels, and cellular cholesterol efflux in subjects with familial low HDL J. Lipid Res., June 1, 2007; 48(6): 1409 - 1416. [Abstract] [Full Text] [PDF]

				M. Van Eck, D. Ye, R. B. Hildebrand, J. Kar Kruijt, W. de Haan, M. Hoekstra, P. C.N. Rensen, C. Ehnholm, M. Jauhiainen, and T. J.C. Van Berkel Important Role for Bone Marrow-Derived Cholesteryl Ester Transfer Protein in Lipoprotein Cholesterol Redistribution and Atherosclerotic Lesion Development in LDL Receptor Knockout Mice Circ. Res., March 16, 2007; 100(5): 678 - 685. [Abstract] [Full Text] [PDF]

				A. Kontush and M. J. Chapman Functionally Defective High-Density Lipoprotein: A New Therapeutic Target at the Crossroads of Dyslipidemia, Inflammation, and Atherosclerosis Pharmacol. Rev., September 1, 2006; 58(3): 342 - 374. [Abstract] [Full Text] [PDF]