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.