Israels L G, Israels E D, Saxena S P
Department of Medicine, Manitoba Institute of Cell Biology, University of Manitoba, Winnipeg, Canada.
Semin Perinatol. 1997 Feb;21(1):90-6. doi: 10.1016/s0146-0005(97)80024-9.
Vitamin K in the fetus and newborn is maintained at levels less than that necessary to achieve full gamma-carboxylation of the K-dependent proteins, including those required for hemostasis. As the infant matures and even into adulthood, there is no significant storage pool for this vitamin, and a K1-deficient state can be produced by placing an adult on a K-deficient diet for 7 to 10 days. Questions arise as to why the level of vitamin K is so rigidly controlled and why the placental gradient in humans and other mammals maintains the fetus in a K-"deficient" state. The evidence is reviewed that suggests that K-dependent proteins are ligands for receptor tyrosine kinases, which, in the rapidly proliferating cell milieu of the fetus, control growth regulation. Increased stimuli may result in growth dysregulation whereas conversely, the further depletion of vitamin K-dependent proteins, as in warfarin toxicity, depletes the required stimuli for normal embryogenesis. These findings argue for the need for tightly controlled levels of vitamin K consistent with normal embryogenesis.
胎儿和新生儿体内的维生素K水平维持在低于使依赖维生素K的蛋白质完全γ-羧化所需的水平，这些蛋白质包括止血所需的蛋白质。随着婴儿的成长，甚至直至成年，这种维生素都没有显著的储存库，并且通过让成年人食用7至10天的维生素K缺乏饮食，就可以产生维生素K1缺乏状态。关于为什么维生素K的水平受到如此严格的控制，以及为什么人类和其他哺乳动物的胎盘梯度会使胎儿处于维生素K“缺乏”状态，出现了一些问题。本文对相关证据进行了综述，这些证据表明依赖维生素K的蛋白质是受体酪氨酸激酶的配体，在胎儿快速增殖的细胞环境中，它们控制生长调节。刺激增加可能导致生长失调，反之，如在华法林毒性中，依赖维生素K的蛋白质进一步耗竭会耗尽正常胚胎发生所需的刺激。这些发现表明需要严格控制维生素K的水平以确保正常胚胎发生。
