URINARY CARNITINE EXCRETION INCREASES DURING EXPERIMENTAL VITAMIN-C DEPLETION OF HEALTHY-MEN

The requirement for ascorbic acid in the biosynthesis of carnitine may provide an explanation for the muscle weakness of scurvy and the basi s for a functional measure of ascorbate status. To determine the relat ionship between vitamin C nutriture and carnitine status in humans, we measured total plasma and urinary carnitine concentrations in samples taken from Two vitamin C depletion/repletion studies performed with h ealthy men on a metabolic unit. Throughout the 13-week studies, the gr oups of nine and eight men consumed a vitamin C-deficient diet that wa s supplemented with ascorbic acid to provide varying intakes of the vi tamin from 5 to 605 mg/day. The subjects attained a state of moderate, nonscorbutic vitamin C deficiency during periods of low vitamin C int ake, as indicated by plasma and leukocyte ascorbate concentrations. Pl asma carnitine and triglyceride concentrations were not affected by th e various vitamin C intakes; however, urinary carnitine excretion was increased during periods of ascorbate deficiency and was inversely rel ated to leukocyte ascorbate concentrations. Vitamin C deficiency incre ases carnitine excretion, but the increased carnitine loss has no effe ct on carnitine status over a period of nearly 9 weeks. Total plasma c arnitine is not a useful functional measure of human vitamin C status. (C) Elsevier Science Inc. 1997.