In higher organisms the carnitine acyltransferases reversibly esterify carnitine which is a primary role of carnitine. With this function it is involved in the beta-oxidation of long-chain fatty acids and in the regulation of CoASH/acyl-CoA ratio in the intracellular compartments. In the intrauterine life there is an increase in stores of carnitine. Many evidences show, that in this growth rate a determinant factor is the materno-fetal transport of carnitine. After interruption of this materno-fetal unit the premature infant depends on exogenous intake. In absence of the exogenous intake due to carnitine free nutrition the tissue carnitine reserves decline in preterm infants. Human milk and many formulas contain carnitine. In carnitine deficiency (insufficiency) syndromes besides of the impairment of oxidation of long chain fatty acids, depending on the degree of carnitine depletion, possible development of multiple deterioration of intracellular processes has been suggested. Impairment of lipid metabolism in preterm infants maintained on carnitine-free feeding regimens seems to be established, in turn, numerous supplemental works suggest a rationale for prevention of decrease of body reserves.