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J. Lipid Res.
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Originally published In Press as doi:10.1194/jlr.M400480-JLR200 on May 16, 2005

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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{dagger}, Matti Jauhiainen{dagger} and Marja-Riitta Taskinen1,*

* Division of Cardiology, Department of Medicine, University of Helsinki, Helsinki, Finland
{dagger} 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


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