Heart mitochondrial metabolism after feeding herring oil to rats and monkeys

Heart mitochondrial oxidation of palmityl CoA and pyruvic acid was studied in rats and in the monkey Macaca fascicularis to determine the effects of feeding partially hydrogenated herring oil. Herring oil glycerides contain cetoleic acid (cis-11-docosenoic) which could have a similar effect to erucic acid (cis-13-docosenoic) in causing a rat cardiomyopathy. The initial rat heart mitochondrial response to dietary cetoleic acid (67% cis, 33% trans) was an in vitro decrease in palmityl CoA oxidation. Pronlonged feeding of cetoleic acid mixture was associated with a significant metabolic adaptation, increasing pyruvate and palmityl CoA oxidation above control levels. In vitro addition of cetoleyl CoA (pure cis isomer) stimulated pyruvate dehydrogenase activity, a possible response to decreased B-oxidation. There was no significant adaptive change in pyruvate or palmityl CoA use in monkeys after prolonged feeding of partially hydrogenated herring oil. Cetoleyl CoA was a good substrate for monkey heart carnitine acyl transferase even in the presence of palmityl CoA. These observations suggest that C22 fatty acids may be metabolized more rapidly in monkey heart than in rat heart. Metabolic differences argue against using the rat as an experimental model for studying possible cardiotoxic effects of docosenoic acids in primates.