Gray T K, Lowe W, Lester G E
Endocr Rev. 1981 Summer;2(3):264-74. doi: 10.1210/edrv-2-3-264.
A model of the maternal-fetal metabolism of vitamin D3 is depicted in Fig. 2. 25-OHD3 of maternal origin is metabolized by the maternal kidneys to the potent metabolite, 1,25-(OH)2D3, which acts on the maternal intestine, kidneys, and skeleton. The maternal kidneys and other organs can produce 24,25-(OH)2D3, although this pathway may be suppressed near the end of gestation. The placenta has selective permeability to the vitamin D3 metabolites, with 25-OHD3 crossing from the mother to the fetus more readily than the dihydroxylated metabolites. The onset of the placental synthesis of 1,25-(OH)2D3 during gestation is unknown. Likewise the regulation of the placental 25-OHD3-1 alpha-hydroxylase is unknown. 1,25-(OH)2D3 of placental origin may enter the maternal or the fetal circulation or act locally on the placenta by inducing the synthesis of proteins involved in the cellular transport of Ca. Perhaps one placenta cell type synthesizes 1,25-(OH)2D3 and another cell type possessing a cytoplasmic receptor for 1,25-(OH)2D3 responds to this metabolite. The function of the 24,25-(OH)2D3 produced by the placenta is unknown. The concentration of free 25-OHD3 and free 1,25-(OH)2D3 in the fetal circulation exceeds the maternal levels due to the differences in the DBP concentrations of the two bloodstreams. The 1,25-(OH)2D3 in the fetal bloodstream may originate from either the placenta or the fetal kidneys. The latter site may not be active in utero due to the hypercalcemia and hyperphosphatemia relative to the maternal levels of these ions. 1,25-(OH)2D3 in the fetal bloodstream acts on those fetal tissues containing cytoplasmic receptors for this metabolite. The intestinal mucosa apparently lacks these receptors until sometime during neonatal life. In contrast, fetal bone cells possess receptors for the 1,25-(OH)2D3. The 24,25-(OH)2D3 in the fetal bloodstream may also be involved in the growth and differentiation of the fetal skeleton. However, the precise role of both metabolites in the fetus remains conjectural.
图2展示了维生素D3的母胎代谢模型。母体来源的25-羟维生素D3（25-OHD3）经母体肾脏代谢为活性代谢产物1,25-二羟维生素D3（1,25-(OH)2D3），后者作用于母体肠道、肾脏和骨骼。母体肾脏及其他器官可产生24,25-二羟维生素D3（24,25-(OH)2D3），不过该途径在妊娠末期可能受到抑制。胎盘对维生素D3代谢产物具有选择性通透性，25-OHD3从母体进入胎儿的速度比二羟化代谢产物更快。妊娠期胎盘合成1,25-(OH)2D3的起始时间尚不清楚。同样，胎盘25-OHD3-1α-羟化酶的调节机制也不清楚。胎盘来源的1,25-(OH)2D3可能进入母体或胎儿循环，或通过诱导参与钙细胞转运的蛋白质合成而在胎盘局部发挥作用。也许一种胎盘细胞类型合成1,25-(OH)2D3，而另一种具有1,25-(OH)2D3细胞质受体的细胞类型对这种代谢产物产生反应。胎盘产生的24,25-(OH)2D3的功能尚不清楚。由于两种血流中维生素D结合蛋白（DBP）浓度的差异，胎儿循环中游离25-OHD3和游离1,25-(OH)2D3的浓度超过母体水平。胎儿血流中的1,25-(OH)2D3可能来源于胎盘或胎儿肾脏。相对于母体这些离子的水平，由于高钙血症和高磷血症，胎儿肾脏这个部位在子宫内可能不活跃。胎儿血流中的1,25-(OH)2D3作用于那些含有这种代谢产物细胞质受体的胎儿组织。直到新生儿期的某个时候，肠黏膜显然还缺乏这些受体。相比之下，胎儿骨细胞具有1,25-(OH)2D3的受体。胎儿血流中的24,25-(OH)2D3也可能参与胎儿骨骼的生长和分化。然而，这两种代谢产物在胎儿体内的确切作用仍属推测。
