Urinary carnitine excretion increases during experimental vitamin C depletion of healthy men

Abstract

The requirement for ascorbic acid in the biosynthesis of carnitine may provide an explanation for the muscle weakness of scurvy and the basis for a functional measure of ascorbate status. To determine the relationship 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 healthy men on a metabolic unit. Throughout the 13-week studies, the groups of nine and eight men consumed a vitamin C-deficient diet that was supplemented with ascorbic acid to provide varying intakes of the vitamin from 5 to 605 mg/day. The subjects attained a state of moderate, nonscorbutic vitamin C deficiency during periods of low vitamin C intake, as indicated by plasma and leukocyte ascorbate concentrations. Plasma carnitine and triglyceride concentrations were not affected by the various vitamin C intakes; however, urinary carnitine excretion was increased during periods of ascorbate deficiency and was inversely related to leukocyte ascorbate concentrations. Vitamin C deficiency increases carnitine excretion, but the increased carnitine loss has no effect on carnitine status over a period of nearly 9 weeks. Total plasma carnitine is not a useful functional measure of human vitamin C status.