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Papers In Press, published online ahead of print September 1, 2002
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Submitted on June 28, 2002
Dept. of Biochemistry 7 Dept. of Medicine and the Cardiovascular Inst., Mount Sinai School of Medicine, New York, NY 10029
Corresponding Author: edward.fisher{at}mssm.edu
ABSTRACT Fatty acids of varying lengths and saturation differentially affect plasma apolipoprotein B100 (apoB100) levels. To identify mechanisms at the level of production, rat hepatoma cells, McA-RH7777, were incubated with 35 S-methionine and either fatty acid-BSA complexes, or BSA alone. There were increases in labeled apoB100 secretion with saturated fatty acids palmitic and myristic (MA) (153+20% and 165+11%, respectively, relative to BSA). Incubation with polyunsaturated docosahexaenoic acid (DHA) decreased secretion to 26+2.0 %, while monounsaturated oleic acid (OA) did not change it. In pulse-chase studies, MA treatment resulted in reduced apoB100 degradation, in agreement with its promotion of secretion. In triglyceride (TG) studies, synthesis was stimulated equally by OA, MA, and DHA, but TG secretion was relatively decreased with MA and DHA. With OA, the majority of newly secreted apoB100-lipoproteins was d<1.006, but with MA, they were much denser (1.063< d). Furthermore, the relative recruitment of newly synthesized TG to lipoproteins was impaired with MA. We conclude that mechanisms for effects of specific dietary fatty acids on plasma lipoprotein levels may include changes in hepatic production. In turn, hepatic production may be regulated by specific fatty acids at the steps of apoB100 degradation and the recruitment of nascent TG to lipoprotein particles.
Revised on August 19, 2002
Accepted on August 20, 2002
Myristic acid treatment of rat hepatoma cells increases the secretion of small denseapoB100-containing lipoproteins by inhibiting the degradation of intracellular apoB andthe utilization of nascent triglycerides for lipoprotein assembly
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