Alkonyi I, Cseko J, Sandor A
University Medical School of Pecs, Biochemical Institute, Hungary.
J Clin Chem Clin Biochem. 1990 May;28(5):319-21.
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.
研究表明,不仅在缺乏抗坏血酸的豚鼠中,而且在部分饥饿的动物中,都会出现肉碱缺乏以及丁酰甜菜碱向肉碱转化受损的情况。我们认为,在这两种营养状态下,相同的机制,即绝对或相对抗坏血酸缺乏,都在起作用。在抗坏血酸缺乏和饥饿状态下,尿排泄增加都极大地促成了豚鼠肉碱缺乏的发展。就排泄大幅增加而言,豚鼠肉碱缺乏类似于人类疾病,可作为其模型。