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

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.

• Authors: Samir S Deeb, Alberto Zambon, Molly C Carr, Amir F Ayyobi, John D Brunzell
• Journal: Journal of lipid research (J Lipid Res) Vol. 44 Issue 7 Pg. 1279-86 (Jul 2003) ISSN: 0022-2275 [Print] United States
• PMID: 12639974 (Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S., Review)

Chemical References

• Lipoproteins, LDL
• Lipase

Topics

• Diabetes Mellitus, Type 2 (genetics)
• Diet
• Female
• Genetic Variation
• Haplotypes
• Humans
• Hyperlipidemia, Familial Combined (genetics)
• Hyperlipidemias (enzymology, genetics)
• Lipase (genetics, physiology)
• Lipoproteins, LDL (metabolism)
• Liver (enzymology)
• Male
• Models, Biological
• Obesity (genetics, metabolism)
• Polymorphism, Genetic
• Promoter Regions, Genetic
• Sex Factors