The ability of guinea pigs to synthesize carnitine at a normal rate from ϵ- N-trimethyllysine or γ-butyrobetaine in vivo is not compromised by experimental vitamin C deficiency

Abstract

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 investigated 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 −) of the carnitine precursors ϵ- N-trimethyllysine or γ-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 μmol · kg body weight −1 · d −1 following supplementation with ϵ- N-trimethyllysine. Likewise, animals in each experimental group showed an increase in the rate of carnitine biosynthesis of 41 to 50 μmol · kg body weight −1 · d −1 after supplementation with γ-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.