Evidence for distinct metabolic utilization of stearic acid in comparison with palmitic and oleic acids in rats

Abstract

Stearic acid, unlike other saturated fatty acids, is possibly hypolipidemic. The rate of plasma clearance and hepatic metabolism of stearic acid, as incorporated into chylomicron lipids, was compared with those of palmitic and oleic acids. Chylomicrons were specifically enriched and labeled in vivo with 14C-stearic acid (SA), palmitic (PA), or oleic acid (OA). Following intravenous injection of rats with labeled chylomicrons, the rates of plasma clearance and hepatic incorporation of the label in triglyceride (TG), phospholipid (PL), and other lipids were compared at 5-, 15-, and 30-min intervals. Stearic acid was cleared at the slowest rate (t1 2 = 19.7 min) compared with PA (t1 2 6.2 min) and OA (t1 2 = 8.1 min). At 30 min. only 68% of the SA dose was removed from the plasma, whereas most of PA (96%) and OA (92%) was cleared. SA and OA were removed by the liver at significantly slower rates compared with PA. At the peak (15 min) of plasma clearance, 17-18% of SA and OA were found in the liver, whereas 37% of PA was taken up by the liver. In the liver, 31.8% of the labeled SA and smaller fractions of PA (15.1%) and OA (6.8%) were present in PL. Conversely, less of the hepatic SA (31.4%) was found in TG, compared with PA (49.0%) and OA (60.4%) in the liver. No significant difference was noted in the relative distributions of 14C in cholesterol and other lipids. Conversion of SA to OA in the liver and intestine was minimal. The data provide new evidence that SA is released slowly from chylomicrons and preferentially utilized for PL synthesis in the liver. The results also suggest that OA is less contributory to hepatic lipogenesis because it is removed by the liver at a much slower rate and better utilized by the extrahepatic tissue than SA and PA. Among the three fatty acids compared, PA is most rapidly taken up and incorporated into TG in the liver. This may stimulate the hepatic synthesis of very low density lipoproteins, (VLDL), contributing to hyperlipidemia. © 1993.