COMPARATIVE LIPOPROTEIN METABOLISM OF MYRISTATE, PALMITATE, AND STEARATE IN NORMOLIPIDEMIC MEN

This project was designed to test the hypothesis that long-chain satur ated fatty acids (myristate, palmitate, and stearate) are metabolized differently in human subjects, and that these differences may therefor e account for the changes in plasma lipoprotein composition when these fatty acids are altered in the diet. Ethyl esters of each of the stab le-isotope-labeled fatty acids (H-2(3)- or H-2(4)-myristate, C-13(16)- palmitate, and C-13(18)-stearate) were fed to five nonhyperlipidemic m en. The concentration of each labeled fatty acid was monitored for up to 72 hours as the fatty acids were assimilated into the lipid compone nts (phospholipid [PL], triglyceride [TG], and cholesteryl ester [CE]) of the plasma lipoproteins (TG-rich lipoproteins [TRL], intermediate density [IDL], low-density [LDL], and high-density lipoprotein [HDL]). Over 95% of the myristate was incorporated into TG, whereas 33% and 9 % of the stearate and 18% and 7% of the palmitate were incorporated in to PL and CE, respectively. The mean residence times (MRTs) for myrist ate in TG (8.6 to 9.9 hours) and PL (6.7 to 10.9 hours) in the individ ual lipoprotein subfractions were significantly shorter than for eithe r palmitate (TG, 12.7 to 15.3 hours; PL, 19.6 to 21.3 hours) or steara te (TG, 10.7 to 15.5 hours; PL, 17.8 to 19.9 hours). The MRTs for stea rate were shorter than for palmitate in PL. These data indicate that T G fatty acid in general, and myristate TG in particular, is the most r apidly cleared of the saturated fatty acids. There was a rapid transfe r of labeled TG and PL between the lipoproteins. We were unable to det ect any significant amount of stearate desaturation or elongation. In conclusion, these data demonstrate that myristate, palmitate, and stea rate are metabolized in unique ways, and that it may therefore be inap propriate to continue to regard all ''saturated fatty acids'' as metab olically similar in clinical studies. Rather, it is important that we elucidate more clearly the specific metabolic pathway of each fatty ac id to understand the mechanisms by which it alters plasma lipoprotein concentrations and composition and influences atherogenesis. Copyright (C) 1996 by W.B. Saunders Company