Influence of dietary fatty acids on liver and adipose tissue lipogenesis and on liver metabolites in meal-fed rats

Rats were trained to eat a fat-free high carbohydrate diet from 800 to 1100 hours each day. After adaptation to meal-eating, the fat- free diet was supplemented with 8% methyl stA©arate(Ci8;o) or 3% methyl linoleate (Ci8:2) for 7 days. Relative to the fat-free group, hepatic utiliza tion of acetate unit equivalents (C2 units) for fatty acid synthesis per mg soluble protein by the Ci8:o group was not significantly altered, whereas Ci8:2 supplementation significantly depressed hepatic fatty acid synthesis. Supplemental Ci8:2 also caused a significant decline in liver fatty acid synthetase and acetyl CoA carboxylase while fat-free and Ci8:o groups dis played similar enzyme activities. Within a treatment, C2 unit utilization tor in vivo fatty acid synthesis was identical to that of acetyl CoA car boxylase and fatty acid synthetase activities in vitro. Therefore, shortly after a meal, the hepatic activities of these two enzymes appear to be functioning at near capacity. Ci8:2 supplementation to the fat-free diet for 7 days caused a 25% decline in glucokinase and pyruvate kinase activ ities, but only pyruvate kinase was significantly depressed. In contrast, citrate cleavage enzyme and fatty acid synthetase were both significantly reduced in activity by 50%. Plasma unesterified fatty acid levels in rats fed Ci8:2 for 5 days were not significantly elevated prior to a meal, al though dietary Ci8:2 did cause a fourfold rise in plasma free linoleate. Quantitation of long chain acyl CoA esters in freeze-clamped liver tissue of rats fed fat-free or fat-free plus 3% Ci8:2 or Ci8:3 diets revealed no con centration differences between treatments either before or after a meal. Similarly, lactate and pyruvate concentrations as well as the lactate: pyru vate ratios were not significantly changed by dietary Ci8:2 or Ci8:3. The inhibitory effects of C18:2 or Ci8;3 appear not to be mediated through changes in total plasma free fatty acid levels, in total hepatic long chain acyl CoA concentration or in hepatic cytosolic redox state. J. Nutr. 107: 1277-1287, 1977.