Experimental
vitamin C deficiency in guinea pigs is associated with low
carnitine concentrations in blood and some tissues.
Ascorbic acid is a cofactor for two
enzymes in the pathway of
carnitine biosynthesis. The effect of experimental
vitamin C deficiency on the ability of guinea pigs to synthesize
carnitine was in animals fed a
vitamin C-deficient diet for 28 days. On days 19 to 28, supplements (0.5 mmol.kg
body weight-1.d-1) of the
carnitine precursors epsilon-N-
trimethyllysine or
gamma-butyrobetaine were administered orally. Ascorbate-supplemented, ascorbate-deficient, and pair-fed (to ascorbate-deficient) animals showed an increase in the rate of
carnitine biosynthesis (as estimated from measured rates of
carnitine excretion) of 32 to 40 mumol.kg body weight-1.d-1 following supplementation with epsilon-N-
trimethyllysine. Likewise, animals in each experimental group showed an increase in the rate of
carnitine biosynthesis of 41 to 50 mumol.kg body weight-1.d-1 after supplementation with
gamma-butyrobetaine. These results indicate that scorbutic guinea pigs are able to synthesize
carnitine at a normal or above-normal rate. For guinea pigs not given a
carnitine precursor supplement, rates of free and total
carnitine excretion for ascorbate-deficient (but not pair-fed) animals were threefold higher than for ascorbate-supplemented animals during days 19 to 28 of the feeding regimen. Thus,
carnitine depletion in
vitamin C deficiency likely is due to excessive urinary excretion of
carnitine and not to a decreased rate of
carnitine biosynthesis.