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Journal of Lipid Research, Vol 37, 693-707, Copyright © 1996 by Lipid Research, Inc.
IJ Goldberg
Although it has been known for over 50 years that lipoprotein lipase (LPL)
hydrolyzes triglyceride in chylomicrons, during the past half decade there
has been a reinterest in the physiologic and pathophysiologic actions of
this enzyme. In part, this has coincided with clinical studies implicating
increased postprandial lipemia as a risk factor for atherosclerosis
development. In addition, the recent creation of genetically altered mice
with hypertriglyceridemia has focused the interest of geneticists and
physiologists on the pathophysiology of triglyceride metabolism. As
reviewed in this article, it is apparent that the lipolysis reaction is
only partially understood. Several factors other than LPL are critical
modulators of this process, in part, because the reaction requires the
lipoproteins to interact with the arterial or capillary wall. Among the
factors that affect this are the apolipoprotein composition of the
particles, the size of the lipoproteins, and how LPL is displayed along the
endothelial luminal surface. Zilversmit's observation that LPL activity is
found in greater amounts in atherosclerotic than normal arteries has led to
a large number of experiments linking LPL with atherogenesis. In medium and
large arteries LPL is found on the luminal endothelial surface and in
macrophage-rich areas within the plaque. LPL actions in both of these
locations probably have major effects on the biology of the blood vessel.
Possible atherogenic actions for this LPL based on in vitro experiments are
reviewed.
REVIEWS
Lipoprotein lipase and lipolysis: central roles in lipoprotein metabolism and atherogenesis
Department of Medicine, Columbia University College of Physicians and Surgeons, New York, NY 10032.
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