Garel J M, Delorme A C, Marche P, Nguyen T M, Garabedian M
Endocrinology. 1981 Jul;109(1):284-9. doi: 10.1210/endo-109-1-284.
Fetomaternal relationships with respect to vitamin D metabolism were investigated in thyroparathyroidectomized (TPTX) pregnant rats, with or without treatment with different vitamin D3 metabolites. Calcium-binding protein (CaBP) in maternal duodenum was used as an index of 1,25-(OH)2D3 status of the mother. Pregnant rats were TPTX on day 12.5 and CaBP was measured on 21.5 days of gestation by RIA in maternal duodenal mucosa and in the fetoplacental unit (placenta, fetal membranes, and fetal intestine). In the duodenum of TPTX mothers, the CaBP concentration was reduced by 50%. This fall was associated with a decrease of 1,25-(OH)2D in maternal plasma. CaBP in maternal duodenum increased by the administration of 1,25-(OH)2D3 or 1,24,25-(OH)3D3. In contrast, 24,25-(OH)2D3 injections to TPTX mothers were ineffective. In both placenta and fetal membranes, CaBPs decreased by 20% in TPTX mothers and were normalized only in 1.25-(OH)2D3-treated TPTX mothers. In the fetal intestine, CaBP variations paralleled those of maternal duodenal CaBP. The data indicate that plasma levels of 1,25-(OH)2D in TPTX pregnant rats are partly under the control of maternal parathyroid glands, and they support that even in pregnancy, the CaBP concentration in maternal duodenum may well reflect the 1,25-(OH)2D status of the mother. The CaBP synthesis in placenta and fetal membranes are vitamin D-dependent, and their regulation differs from that of intestinal CaBP. It app]ears that 1 alpha-hydroxylase activities of the fetoplacental unit (placenta and fetal kidney) are blunted in TPTX animals and that CaBP synthesis in the fetus depends on the presence of 1 alpha-hydroxylated vitamin D3 metabolites in the mother.
在切除甲状腺和甲状旁腺(TPTX)的怀孕大鼠中,研究了维生素D代谢方面的母胎关系,这些大鼠接受或未接受不同维生素D3代谢物的治疗。母体十二指肠中的钙结合蛋白(CaBP)用作母亲1,25-(OH)2D3状态的指标。怀孕大鼠在第12.5天接受TPTX手术,并在妊娠第21.5天通过放射免疫分析(RIA)测量母体十二指肠黏膜和胎儿胎盘单位(胎盘、胎膜和胎儿肠道)中的CaBP。在TPTX母亲的十二指肠中,CaBP浓度降低了50%。这种下降与母体血浆中1,25-(OH)2D的减少有关。通过给予1,25-(OH)2D3或1,24,25-(OH)3D3,母体十二指肠中的CaBP增加。相比之下,给TPTX母亲注射24,25-(OH)2D3无效。在胎盘和胎膜中,TPTX母亲的CaBPs降低了20%,只有接受1,25-(OH)2D3治疗的TPTX母亲才恢复正常。在胎儿肠道中,CaBP的变化与母体十二指肠CaBP的变化平行。数据表明,TPTX怀孕大鼠血浆中1,25-(OH)2D的水平部分受母体甲状旁腺的控制,并且支持即使在怀孕期间,母体十二指肠中的CaBP浓度也很可能反映母亲的1,25-(OH)2D状态。胎盘和胎膜中的CaBP合成依赖于维生素D,并且它们的调节与肠道CaBP不同。似乎TPTX动物中胎儿胎盘单位(胎盘和胎儿肾脏)的1α-羟化酶活性减弱,并且胎儿中的CaBP合成取决于母亲体内1α-羟化维生素D3代谢物的存在。