Plasma Carnitine of the Premature Infant

Premature infants have been shown to exhibit fat intolerance with the administration of exogenous lipid, especially intravenous lipid. Carnitine is required for the efficient oxidation of long-chain fatty acids. Since infants have been reported to be unable to synthesize carnitine, the carnitine and lipid status was investigated in a series of premature infants throughout the entire period of hospitalization. At birth, the plasma carnitine of three groups of appropriate for gestational (AGA) premature infants (n=36), was compared with full term infants (n=10), and with maternal and umbilical cord plasma carnitine levels. The plasma concentrations of carnitine, triglyceride, and in some cases free fatty acids, were determined on each of the premature infants on days 0-5, 7, and then weekly until discharge. The plasma concentration of carnitine and lipid were also determined prior to, and after, the initiation of various types of infant feedings. The feedings consisted of both carnitine-free and carnitine-containing formula/infusates. The relationship of the levels of carnitine and lipid were analyzed between groups to determine if lipid intolerance was associated with a depressed carnitine concentration. The plasma levels of carnitine and lipid were also analyzed to determine their relationship with carnitine, fat, and in the case of triglyceride, with calorie intake.

Results showed that infant plasma carnitine levels at birth were directly related to the maternal plasma carnitine concentration. The infant plasma carnitine level was higher in the younger infants when compared with the older prematures and full term infants. All groups exhibited a decrease of the ratio of non-esterified carnitine to acid-soluble acylcarnitines soon after birth, which indicated metabolism of lipid by B-oxidation. Most of the infants required an exogenous source of carnitine for the maintenance of the plasma carnitine level. However two infants showed a slight elevation of plasma carnitine while on a carnitine-free diet. This may have been due to either an active biosynthesis of carnitine, a release of carnitine from red blood cells, or a release of tissue carnitine.

All infants responded to dietary carnitine intake with an elevation of the plasma carnitine level. The plasma triglyceride level was directly related to calorie intake, but correlated to fat intake only in the the older premature infants.

A significant negative relationship between the plasma levels of carnitine and triglyceride did not exist in any group. However at the time of peak depression of plasma carnitine, the intake of intravenous lipid and long-chain fatty acids was relatively low. During this time most infants received medium-chain triglycerides as the primary source of exogenous fat, which might explain this unexpected result. Therefore it appears that premature infants tolerate intravenous lipid doses of at least 1.0 - 1.5 g/kg/day and diets which contain a high percentage of total fat from medium-chain triglycerides without evidence of fat intolerance even when they are maintained on a carnitine-free diet.