(Circulation. 2000;102:1600.)
© 2000 American Heart Association, Inc.
Editorial |
From the Atherosclerosis Research Unit, Division of Cardiology, University of Southern California School of Medicine, Los Angeles.
Correspondence to Howard N. Hodis, MD, Atherosclerosis Research Unit, Division of Cardiology, University of Southern California School of Medicine, 2250 Alcazar Street, CSC 132, Los Angeles, CA 90033.
It has been >55 years since Hahn1 first observed that the intravenous injection of heparin abolished postprandial lipemia in dogs; subsequently, Korn and Quigley2 identified the factor released by intravenous heparin as a triglyceride lipase. Since that time, the putative role of lipoprotein lipase in atherosclerosis has expanded tremendously.
Lipoprotein lipase is a key enzyme in the regulation of lipid fuel disposal,3 and it provides fatty acids for tissue utilization by catalyzing the hydrolysis of triacylglycerol circulating in triglyceride-rich lipoproteins. Anchored to the surface of the capillary endothelium by glycosaminoglycans, lipoprotein lipase hydrolyzes plasma chylomicrons and VLDL to remnant particles. As such, lipoprotein lipase is the rate-limiting enzyme responsible for the removal of plasma triglyceride-rich lipoproteins from the circulation. Although expressed in most tissues of the body, in particular, skeletal and heart muscle and adipose tissue, lipoprotein lipase is also expressed and secreted by macrophages. Lipoprotein lipase is important for the transfer of phospholipids and apolipoproteins to HDL and, thus, is critical for the formation of this particle.4 Apolipoprotein C-II is an essential cofactor for the activation of lipoprotein lipase activity, whereas apolipoprotein C-III inhibits activity.5
A number of polymorphisms in the lipoprotein lipase gene have been
associated with varying degrees of plasma lipoprotein levels and the
severity of coronary artery disease.6 Low levels
of lipoprotein lipase activity, as seen with a partial deficiency of
lipoprotein lipase, have been associated with the progression of
coronary atherosclerosis.7
Decreased lipoprotein lipase activity and the resultant elevated
triglyceride levels and reduced HDL cholesterol
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