Comparative lipoprotein metabolism of myristate, palmitate, and stearate in normolipidemic men.

This project was designed to test the hypothesis that long-chain saturated fatty acids (myristate, palmitate, and stearate) are metabolized differently in human subjects, and that these differences may therefore account for the changes in plasma lipoprotein composition when these fatty acids are altered in the diet. Ethyl esters of each of the stable-isotope-labeled fatty acids (2H3- or 2H4-myristate, 13C16-palmitate, and 13C18-stearate) were fed to five nonhyperlipidemic men. The concentration of each labeled fatty acid was monitored for up to 72 hours as the fatty acids were assimilated into the lipid components (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 into PL and CE, respectively. The mean residence times (MRTs) for myristate in TG (8.6 to 9.9 hours) and PL (6.7 to 10.9 hours) in the individual lipoprotein subfractions were significantly shorter than for either palmitate (TG, 12.7 to 15.3 hours; PL, 19.6 to 21.3 hours) or stearate (TG, 10.7 to 15.5 hours; PL, 17.8 to 19.9 hours). The MRTs for stearate were shorter than for palmitate in PL. These data indicate that TG fatty acid in general, and myristate TG in particular, is the most rapidly cleared of the saturated fatty acids. There was a rapid transfer of labeled TG and PL between the lipoproteins. We were unable to detect any significant amount of stearate desaturation or elongation. In conclusion, these data demonstrate that myristate, palmitate, and stearate are metabolized in unique ways, and that it may therefore be inappropriate to continue to regard all "saturated fatty acids" as metabolically similar in clinical studies. Rather, it is important that we elucidate more clearly the specific metabolic pathway of each fatty acid to understand the mechanisms by which it alters plasma lipoprotein concentrations and composition and influences atherogenesis.