Abstract
Lipoprotein metabolism involves two major steps (Eisenberg 1990). First, triglyceride (TG) rich lipoproteins bind transiently to lipoprotein lipase (LPL) at the vascular endothelium (Fig. 1). The enzyme rapidly hydrolyzes triglycerides, which accomplishes two things (Eckel 1989): it enables the tissues to utilize fatty acids from the lipoproteins, and it transforms large TG-rich lipoproteins (chylomicrons and very low density lipoproteins, VLDL) into cholesterol-rich remnant lipoproteins. This process is completed within the space of a few minutes to a few hours after the lipoproteins have entered circulation. Some of the remnants are rapidly removed from the circulation by receptor-mediated endocytosis, but some are transformed into low-density lipoproteins (LDL) and high-density lipoproteins (HDL). Subjects with genetic deficiency of LPL demonstrate that the enzyme is indeed necessary for these reactions; there is massive accumulation of TG-rich lipoproteins in plasma and low levels of LDL and HDL (Brunzell et al. 1986).
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Olivecrona, T., Olivecrona, G. (1994). Lipoprotein Lipase and Hepatic Lipase. In: Schettler, G., Habenicht, A.J.R. (eds) Principles and Treatment of Lipoprotein Disorders. Handbook of Experimental Pharmacology, vol 109. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-78426-2_6
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