THE ABILITY OF GUINEA-PIGS TO SYNTHESIZE CARNITINE AT A NORMAL RATE FROM EPSILON-N-TRIMETHYLLYSINE OR GAMMA-BUTYROBETAINE IN-VIVO IS NOT COMPROMISED BY EXPERIMENTAL VITAMIN-C-DEFICIENCY

Experimental vitamin C deficiency in guinea pigs is associated with lo w 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 guin ea pigs to synthesize carnitine was investigated in animals fed a vita min C-deficient diet for 28 days. On days 19 to 28, supplements (0.5 m mol . kg body weight(-1) . d(-1)) of the carnitine precursors epsilon- N-trimethyllysine or gamma-butyrobetaine were administered orally. Asc orbate-supplemented, ascorbate deficient, and pair-fed (to ascorbate d eficient) animals showed an increase in the rate of carnitine biosynth esis (as estimated from measured rates of carnitine excretion) of 32 t o 40 mu mol . kg body weight(-1) d(-1) following supplementation with epsilon-N-trimethyilysine. Likewise, animals in each experimental grou p showed an increase in the rate of carnitine biosynthesis of 41 to 50 mu mol . kg body weight(-1) . d(-1) after supplementation with gamma- butyrobetaine. These results indicate that scorbutic guinea pigs are a ble to synthesize carnitine at a normal or above-normal rate. For guin ea pigs not given a carnitine precursor supplement, rates of free and total carnitine excretion for ascorbate-deficient (but not pair-fed) a nimals were threefold higher than for ascorbate-supplemented animals d uring days 19 to 28 of the feeding regimen. Thus, carnitine depletion in vitamin C deficiency likely is due to excessive urinary excretion o f carnitine and not to a decreased rate of carnitine biosynthesis. Cop yright (C) 1995 by W.B. Saunders Company