Most lipid emulsions for parenteral feeding of premature infants are based on long-chain triacylglycerols (LCTs), but inclusion of medium-chain triacylglycerols (MCTs) might provide a more readily oxidizable energy source. The influence of these emulsions on fatty acid composition and metabolism was studied in 12 premature neonates, who were randomly assigned to an LCT emulsion (control) or an emulsion with a mixture of MCT and LCT (1:1). On study day 7, all infants received [

The prevalence of the Leiden mutation was tested in 50 mothers of premature infants and in 56 mothers of intrauterine-growth-retarded neonates. The prevalence of the Leiden mutation was 7.2% in the mothers of growth-retarded neonates and 18% in the group of mothers of premature infants, the latter being significantly higher than the 6.3% prevalence of this mutation in healthy Hungarian subjects (p < 0.01). In spite of the relatively small number of mothers examined, the unexpected finding may call attention to a hitherto unknown relationship.

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6-N-Trimethyl-[d₉]-L-lysine (dTML), the labeled form of a mammalian carnitine precursor, was administered to two groups of premature infants. Although the urinary output of dTML significantly increased in the low-dose-treated group (100 μmol/day), this amount did not affect the urinary output or plasma levels of carnitine and carnitine esters. In the second group of infants, after administration of 500 μmol dTML the plasma-free carnitine concentration increased (from 9.95 ± 0.63 to 12.9 ± 0.87 nmol/ml, p > 0.05) with a significant increase in the urinary excretion of free carnitine on the day of dTML administration and on the posttreatment day (from 4.79 ± 1.36 to 9.85 ± 1.18 and to 17.5 ± 2.31 μmol/day, respectively). Analysis of urine using fast atom bombardment mass spectrometry (FAB-MS) revealed only the presence of the dTML in the urine of the newborns; no change was detected in the relative abundance of any other carnitine precursor. Surprisingly, in the second group, which received the higher dose of dTML supplement, only the signal intensity of the unlabeled carnitine increased after dTML administration; no new peak appeared in the urine that would correspond to the de novo synthesized carnitine containing the stable isotope-labeled trimethyl group of dTML. Thus, the FAB-MS analysis clearly demonstrated that contrary to the likely prediction, the 270% extra free carnitine output was a consequence of a dose-dependent dTML-induced depletion of the free carnitine reserves from the newborns. The absence of the incorporation of the label from dTML into carnitine strongly suggests that circulating TML is not the precursor of carnitine in premature infants.