Abstract
AbstractUnsaturated long‐chain fatty acids are oxidized more rapidly than are saturated fatty acids of similar chain length in intact animals and isolated mitochondria. Gamma‐oxidation of the 3‐dodecenoic acid intermediate in beta‐oxidation of oleate would yield propionate which is metabolized via methylmalonate.14C‐labeled fatty acids were administered to intact rats, muscle homogenates and lysed mitochondria. Methylmalonate, succinate and CO2 were isolated and14C determined. Incorporation of U‐14C‐linoleate into methylmalonate in vitro was 20 times greater than from U‐14C‐palmitate. Rats fed 20% corn oil grew more slowly on B12 deficient than B12 sufficient diets. Biotin and vitamin B12 deficiencies were found to decrease the in vivo metabolism of linoleate. These data suggest that one pathway of linoleate oxidation has methylmalonate as an intermediate.
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