Evidence that the development of hepatic fatty acid oxidation at birth in the rat is concomitant with an increased intramitochondrial CoA concentration


Correspondence to P. Ferre, Centre de Recherches sur la Nutrition du CNRS, 9 Rue Jules Hetzel, F-92190 Meudon-Bellevue, France


The development of hepatic fatty acid oxidation during the perinatal period in the rat was studied using isolated mitochondria. Ketone body synthesis from substrates entering at different levels of β-oxidation was 2–3 times lower in mitochondria isolated from term-fetal liver than in 16-h-old newborn or adult liver mitochondria. The low rate of palmitoyl-l-carnitine oxidation in term-fetal mitochondria was linked neither to the low capacity of the respiratory chain nor to the removal of acetyl-CoA in the hydroxymethylglutaryl-CoA synthase pathway. The 2.5-times lower concentration of CoA found in term-fetal liver mitochondria when compared to 16-h-old or adult liver mitochondria might be the factor responsible for the low rate of fatty acid oxidation in term-fetal liver mitochondria.