J. Lipid Res. Neurobiology of Lipids (ISSN1683-5506)
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A more recent version of this article appeared on August 1, 2005

Papers In Press, published online ahead of print May 16, 2005
J. Lipid Res., doi:10.1194/jlr.M400480-JLR200
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Submitted on December 7, 2004
Revised on April 13, 2005
Accepted on May 4, 2005

Hypertriglyceridemia is associated with prebeta -HDL levels in subjects with familial low HDL

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

Department of Medicine, University of Helsinki, Helsinki 00290

Corresponding Author: Marja-Riitta.Taskinen{at}helsinki.fi

Preß-HDL particles act as the primary acceptors of cellular cholesterol in the reverse cholesterol transport (RCT) process. 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 serum preß-HDL concentration as compared to the normolipidemic subjects (17.4 ± 7.2 vs. 23.4 ± 7.8 mg of 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 the subjects with familial low HDL. The activities of cholesterol ester transfer protein (CETP) and hepatic lipase (HL) were markedly increased in the 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.


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