Abstract

1. 1. Acetyl-CoA carboxylase activity and the capacity for fatty acid synthesis were measured in the livers from normal, pregnant, and fetal rabbits. 2. 2. The activity of acetyl-CoA carboxylase decreased in the pregnant animals and showed very low enzyme values in fetal liver. On the other hand, fetal liver exhibited a maximal capacity for the synthesis of fatty acids from [ 14C] acetyl-CoA. 3. 3. Long-term administration of insulin produced a clear diminution of the acetyl-CoA carboxylase activity as well as an increase of the fatty acid synthesis capacity in adult liver. 4. 4. Evidence was obtained that in the fetal liver of rabbits an elongation mechanism controls the synthesis of fatty acids whereas the adult liver possesses a de novo mechanism. 5. 5. The effect of different concentrations of NADH and NADPH was measured on both enzyme capacities. NADPH had a marked stimulatory effect on acetyl-CoA carboxylase of adult liver, but it had hardly any effect on the enzyme activity of fetal liver. 6. 6. The results of varying the relative concentrations of either NADPH and citrate or malonyl-CoA and citrate on the acetyl-CoA carboxylase activity suggest that the nucleotide removes a certain inhibitory effect of malonate by promoting its utilization for the synthesis of fatty acids. The inhibitory activity of malonyl-CoA requires the presence of the activated form of the enzyme. 7. 7. The influence of avidin was also measured on acetyl-CoA carboxylase and the synthesis of fatty acids from [ 14C] acetyl-CoA in liver from either control adult or fetal rabbits. All results strengthen the idea of a different participation of the various mechanisms for the fatty acid synthesis in either adult or fetal liver.

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