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Originally published In Press as doi:10.1194/jlr.R200017-JLR200 on March 16, 2003

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Journal of Lipid Research, Vol. 44, 1279-1286, July 2003
Copyright © 2003 by American Society for Biochemistry and Molecular Biology

Review

Hepatic lipase and dyslipidemia

: interactions among genetic variants, obesity, gender, and diet

Samir S. Deeb1,*, Alberto Zambon{dagger}, Molly C. Carr{dagger}, Amir F. Ayyobi{dagger} and John D. Brunzell{dagger}

* Divisions of Medical Genetics, Department of Medicine, University of Washington, Seattle, WA 98195
{dagger} Metabolism, Endocrinology, and Nutrition, Department of Medicine, University of Washington, Seattle, WA 98195

1 To whom correspondence should be addressed. e-mail: sdeeb{at}u.washington.edu

Hepatic lipase (HL) plays a central role in LDL and HDL remodeling. High HL activity is associated with small, dense LDL particles and with reduced HDL2 cholesterol levels. HL activity is determined by an HL gene promoter polymorphism, by gender (lower in premenopausal women), and by visceral obesity with insulin resistance. The activity is affected by dietary fat intake and selected medications. There is evidence for an interaction of the HL promoter polymorphism with visceral obesity, dietary fat intake, and with lipid-lowering medications in determining the level of HL activity.

The dyslipidemia with high HL activity is a potentially proatherogenic lipoprotein profile in the metabolic syndrome, in Type 2 diabetes, and in familial combined hyperlipidemia.

Supplementary key words hepatic lipase genetics • atherosclerosis • hyperlipidemia


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