Black A L, Guirard B M, Snell E E
J Nutr. 1978 Apr;108(4):670-7. doi: 10.1093/jn/108.4.670.
Current belief that vitamin B6 deficiency causes depletion of muscle phosphorylase in animals appears to be erroneous. We present evidence that vitamin B6 deficiency is ineffective in reducing total phosphorylase in gasttocnemius muscle of young rats over a period of at least 8 weeks. Rats that had accumulated high levels of muscle phosphorylase while ingesting diets containing normal or excess amounts of the vitamin retained their phosphorylase after transfer to a vitamin B6 deficient diet. Prolonged deficiency did ultimately lead to enzyme depletion but this was after anorexia had developed and weight loss had occurred. When rats were partially starved for 1 to 4 days (fed 10% of normal energy intake) they lost muscle phosphorylase while retaining alanine and aspartate aminotransferases. When totally starved, the rats lost more phosphorylase than during partial starvation, but completely retained alanine aminotransferase, and lost some aspartate aminotrasferase. We conclude that the behavior of muscle phosphorylase is consistent with the Krebs-Fischer proposal that it acts as a reservoir for vitamin B6 and that starvation, but not vitamin B6 deficiency per se, causes depletion of muscle phosphorylase. It appears that phosphorylase may function as an adjunct ot adipose tissue necessary for the animal to efficiently meet the exigencies of starvation.
目前认为维生素B6缺乏会导致动物肌肉磷酸化酶耗竭的观点似乎是错误的。我们提供的证据表明，在至少8周的时间里，维生素B6缺乏对降低幼鼠腓肠肌中的总磷酸化酶没有效果。在摄入含有正常或过量该维生素的日粮时积累了高水平肌肉磷酸化酶的大鼠，在转至维生素B6缺乏日粮后仍保留其磷酸化酶。长期缺乏最终确实导致了酶的耗竭，但这是在出现厌食和体重减轻之后。当大鼠部分饥饿1至4天（给予正常能量摄入量的10%）时，它们失去了肌肉磷酸化酶，同时保留了丙氨酸和天冬氨酸转氨酶。当完全饥饿时，大鼠失去的磷酸化酶比部分饥饿时更多，但完全保留了丙氨酸转氨酶，并失去了一些天冬氨酸转氨酶。我们得出结论，肌肉磷酸化酶的行为与克雷布斯 - 费舍尔的提议一致，即它作为维生素B6的储存库，并且是饥饿而非维生素B6本身缺乏导致肌肉磷酸化酶的耗竭。看来磷酸化酶可能作为动物有效应对饥饿紧急情况所需的脂肪组织的辅助物发挥作用。
