It was shown that carnitine deficiency and an impairment of the conversion of butyrobetaine
into carnitine develops not only in ascorbic acid-deficient guinea-pigs but also in
partially starved animals. We propose that the same mechanism, an absolute or relative
ascorbic acid deficiency, is operating in both nutritional states. An increased urinary
excretion greatly contributes to the development of carnitine deficiency in guinea-pigs,
both in ascorbic acid deficiency and starvation. With respect to the greatly increased
excretion, guinea-pig carnitine deficiency resembles the human disorder and may serve
as model for it.