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Invited Review: Lipoprotein Lipase and Triglyceride‐Rich Lipoprotein Metabolism
Author(s) -
Miles John M.,
Park Yongsoon,
Harris William S.
Publication year - 2001
Publication title -
nutrition in clinical practice
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.725
H-Index - 71
eISSN - 1941-2452
pISSN - 0884-5336
DOI - 10.1177/088453360101600502
Subject(s) - chylomicron , lipoprotein lipase , triglyceride , hypertriglyceridemia , medicine , endocrinology , lipoprotein , biochemistry , very low density lipoprotein , cholesterol , adipose tissue , chemistry
Lipoprotein lipase (LPL) is the key enzyme responsible for fat storage. It hydrolyzes triglyceride contained in circulating very low‐density lipoproteins and chylomicrons; the fatty acids that are produced are transported locally into tissues, whereas glycerol is released into the circulation. Abnormalities in LPL activity have been described in a variety of hypertriglyceridemic states, including diabetes mellitus, and in some situations may contribute to atherosclerosis. Previous in vivo studies suggest that LPL is saturable, with maximum rates of fatty acid transport and storage occurring at plasma triglyceride concentrations in the 300 to 400 mg/dL range. At higher triglyceride concentrations, significant nonenzymatic uptake, primarily by the reticuloendothelial system, can occur. Impaired neutrophil, platelet, and pulmonary function have been described in association with IV infusion of lipid emulsions at high rates. There is no evidence that lipid emulsions produce any of these adverse effects at plasma triglyceride concentrations below 300 to 400 mg/dL. Inordinate hypertriglyceridemia can usually be avoided by limiting lipid infusion rates to 30 to 50 mg/kg‐h, a rate sufficient to meet nutritional needs under most conditions.