Carnitine in the perinatal metabolism of lipids. I. Relationship between maternal and fetal plasma levels of carnitine and acylcarnitines.

Since premature infants have a limited capacity for fatty acid oxidation, supplementation with carnitine may improve their utilization of fat. Documentation of the source and extent of fetal carnitine reserves should explain the possible need for exogenous carnitine in the neonate. Correlation between free carnitine concentration in maternal and umbilical arterial plasma at birth (r = .45, P less than .01) indicates that the initial concentration of free carnitine in the newborn depends on the maternal level. Thin-layer chromatography shows more gamma-butyrobetaine in maternal than umbilical arterial plasma indicating higher availability of the precursor of carnitine biosynthesis. Elevated fatty acid oxidation in maternal tissues seems to be reflected by larger amounts of long-chain acylcarnitines in maternal plasma. Short-chain acylcarnitines, mainly acetylcarnitine, are higher in the umbilical vein than in maternal plasma (P less than .01) indicating that the conceptus (the placenta or fetus) is either producing more or utilizing less acetylcarnitine. Plasma levels of carnitine rapidly decrease in premature newborns during the first three days after birth if no exogenous carnitine is given (P less than .001), while no significant changes of total carnitine were detected in adult patients on total parenteral alimentation for one week. This difference indicates lower carnitine depots or limited capacity for carnitine biosynthesis in neonates. The possibility still requires further investigation that the development of the optimal rate of fatty acid oxidation in human newborns, as well as in other newborn mammals, may depend on the supply of exogenous carnitine.