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肝脂肪酶与血脂异常:基因变异、肥胖、性别和饮食之间的相互作用

Hepatic lipase and dyslipidemia: interactions among genetic variants, obesity, gender, and diet.

作者信息

Deeb Samir S, Zambon Alberto, Carr Molly C, Ayyobi Amir F, Brunzell John D

机构信息

Divisions of Medical Genetics, Department of Medicine, University of Washington, Seattle, WA 98195, USA.

出版信息

J Lipid Res. 2003 Jul;44(7):1279-86. doi: 10.1194/jlr.R200017-JLR200. Epub 2003 Mar 16.

Abstract

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.

摘要

肝脂酶(HL)在低密度脂蛋白(LDL)和高密度脂蛋白(HDL)重塑过程中起着核心作用。高HL活性与小而致密的LDL颗粒以及HDL2胆固醇水平降低有关。HL活性由HL基因启动子多态性、性别(绝经前女性较低)以及伴有胰岛素抵抗的内脏肥胖所决定。该活性受膳食脂肪摄入和某些药物的影响。有证据表明,在决定HL活性水平方面,HL启动子多态性与内脏肥胖、膳食脂肪摄入以及降脂药物之间存在相互作用。HL活性高的血脂异常在代谢综合征、2型糖尿病和家族性混合性高脂血症中是一种潜在的促动脉粥样硬化脂蛋白谱。

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