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A more recent version of this article appeared on July 1, 2003
Papers In Press, published online ahead of print March 16, 2003
J. Lipid Res., doi:10.1194/jlr.R200017-JLR200
Submitted on October 7, 2002
Revised on March 4, 2003
Accepted on March 5, 2003
Hepatic lipase and dyslipidemia: Interactions between genetic variants, obesity, gender and diet
Samir S. Deeb, Alberto Zambon, Molly C. Carr, Amir F. Ayyobi, and John D. Brunzell
Medicine Dept., Division of Medical Genetics, University of Washington, Seatle, WA 98195
Corresponding Author: 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 a 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.

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Copyright © 2003 by the American Society for Biochemistry and Molecular Biology.
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