Lipoprotein lipase and atherosclerosis

Abstract 

Lipoprotein lipase (LPL) is a key enzyme in catabolism of plasma lipoprotein triglycerides (TGs), and in that capacity has a salutary influence on plasma HDL, and thus appears to be antiatherogenic. However, the non-catalytic functions of LPL, such as lipoprotein bridging and selective uptake of lipoprotein cholesteryl ester, are regarded as proatherogenic. The balance between the pro and antiatherogenic attributes of LPL is evaluated on the basis of recent evidence derived from transgenic animals and from studies of common LPL mutations in man. This review also includes recently accrued information on the role of nuclear receptors and their ligands and agonists in regulation of LPL in various organs. The studies reviewed are not only of academic interest, but may also have practical applications in development of agents that may regulate LPL activity in humans.

Keywords: Macrophage, Transgenic mice, Rabbits, PPAR, LPL mutations, LPL atherogenicity, LPL antiatherogenicity