Furukawa Y, Numazawa T, Fukazawa H, Ikai M, Ohinata K, Maebashi M, Kim D H, Ito M, Komai M, Kimura S
Department of Applied Biological Chemistry, Faculty of Agriculture, Tohoku University, Sendai, Japan.
Int J Vitam Nutr Res. 1993;63(2):129-34.
The biological consequences of biotin deficiency in rats were investigated using osteogenic disorder Shionogi rats which have a hereditary defect in ascorbic acid synthesizing ability. Decrease of liver ascorbic acid content and fasting plasma glucose and an increase of plasma non-esterified fatty acid (NEFA) appeared in biotin deficient rats fed a diet containing 200 mg ascorbic acid per 100 g diet, compared with the pair fed control. On the other hand, in the case of rats fed a diet containing 500 mg ascorbic acid, although the clinical features of biotin deficiency developed, the ascorbic acid contents of liver and adrenal gland increased in comparison with those of AsA 200 mg groups, and the alterations of plasma levels of glucose and NEFA were improved partially in glucose and greatly in NEFA, respectively. This suggests that ascorbic acid may be consumed in the improvement of the metabolic impairments induced by biotin deficiency.
利用具有抗坏血酸合成能力遗传性缺陷的成骨障碍史氏大鼠，研究了大鼠生物素缺乏的生物学后果。与配对喂养的对照组相比，在每100克饲料含200毫克抗坏血酸的饲料喂养的生物素缺乏大鼠中，肝脏抗坏血酸含量、空腹血糖降低，血浆非酯化脂肪酸（NEFA）增加。另一方面，在每100克饲料含500毫克抗坏血酸的饲料喂养的大鼠中，虽然出现了生物素缺乏的临床特征，但与抗坏血酸200毫克组相比，肝脏和肾上腺的抗坏血酸含量增加，血浆葡萄糖和NEFA水平的变化分别在葡萄糖方面得到部分改善，在NEFA方面得到极大改善。这表明抗坏血酸可能在改善生物素缺乏引起的代谢损伤中被消耗。
