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Journal of Lipid Research, Vol. 43, 1352-1362, September 2002
Copyright © 2002 by Lipid Research, Inc.
Thematic Review |
Hepatic lipase
: a pro- or anti-atherogenic protein?
,
* Departments of Biochemistry, Erasmus MC, Erasmus University Rotterdam, Rotterdam, The Netherlands
Internal Medicine, Erasmus MC, Erasmus University Rotterdam, Rotterdam, The Netherlands
Clinical Chemistry, Erasmus MC, Erasmus University Rotterdam, Rotterdam, The Netherlands
1 To whom correspondence should be addressed. e-mail: jansen{at}bc1.fgg.eur.nl
Hepatic lipase (HL) plays a role in the metabolism of pro- and anti-atherogenic lipoproteins affecting their plasma level and composition. However, there is controversy regarding whether HL accelerates or retards atherosclerosis. Its effects on different lipoprotein classes show that, potentially, HL may promote as well as decrease atherogenesis. Studies in animals with genetically modulated HL expression show that it depends on the model used whether HL acts pro- or anti-atherogenic. In humans, HL activity seems to correlate inversely with atherosclerosis in (familial) hypercholesterolemia, and positively in hypertriglyceridemia. In normolipidemia, HL activity is weakly associated with coronary artery disease (CAD). Genetically low or absent HL activity is usually associated with increased CAD risk, especially if plasma lipid transport is impaired due to other factors. Since HL promotes the uptake of lipoproteins and lipoprotein-associated lipids, HL may affect intracellular lipid content.
We hypothesize that the prime role of HL is to maintain, in concert with other factors (e.g., lipoprotein receptors), intracellular lipid homeostasis. This, and the uncertainties about its impact on human atherosclerosis, makes it difficult to predict whether HL is a suitable target for intervention to lower CAD risk. First, the physiological meaning of changes in HL activity under different conditions should be clarified.
Abbreviations: apo, apolipoprotein; CAD, coronary artery disease; FH, familial hypercholesterolemia; HL, hepatic lipase; RCT, reverse cholesterol transfer; LDLR, LDL receptor
Supplementary key words coronary heart disease • risk factor • lipoprotein metabolism • lipid homeostasis • liver • hyperlipidemia • obesity
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