关键词: neonates obesity placenta pregnancy vitamin D vitamin D metabolism vitamin D-binding protein

Mesh : Humans Female Pregnancy Placenta / metabolism drug effects Vitamin D / administration & dosage analogs & derivatives blood Dietary Supplements Infant, Newborn Adult Vitamin D Deficiency / drug therapy 25-Hydroxyvitamin D3 1-alpha-Hydroxylase / genetics metabolism Vitamin D3 24-Hydroxylase / genetics metabolism Vitamin D-Binding Protein / genetics metabolism Receptors, Calcitriol / genetics metabolism Low Density Lipoprotein Receptor-Related Protein-2 / metabolism genetics Maternal Nutritional Physiological Phenomena Receptors, Cell Surface

来  源:   DOI:10.3390/nu16132145   PDF(Pubmed)

Abstract:
Vitamin D (vitD) deficiency (25-hydroxy-vitamin D < 50 nmol/L) is common in pregnancy and associated with an increased risk of adverse pregnancy outcomes. High-dose vitD supplementation is suggested to improve pregnancy health, but there is limited knowledge about the effects on placental vitD transport and metabolism and the vitD status of newborns. Comparing the current standard maternal supplementation, 10 µg/day to a 90 µg vitD supplement, we investigated placental gene expression, maternal vitD transport and neonatal vitD status. Biological material was obtained from pregnant women randomized to 10 µg or 90 µg vitD supplements from week 11-16 onwards. Possible associations between maternal exposure, neonatal vitD status and placental expression of the vitD receptor (VDR), the transporters (Cubilin, CUBN and Megalin, LRP2) and the vitD-activating and -degrading enzymes (CYP24A1, CYP27B1) were investigated. Maternal vitD-binding protein (VDBP) was determined before and after supplementation. Overall, 51% of neonates in the 10 µg vitD group were vitD-deficient in contrast to 11% in the 90 µg group. High-dose vitD supplementation did not significantly affect VDBP or placental gene expression. However, the descriptive analyses indicate that maternal obesity may lead to the differential expression of CUBN, CYP24A1 and CYP27B1 and a changed VDBP response. High-dose vitD improves neonatal vitD status without affecting placental vitD regulation.
摘要:
维生素D(vitD)缺乏(25-羟基维生素D<50nmol/L)在妊娠中很常见,并且与不良妊娠结局的风险增加有关。建议补充高剂量vitD以改善妊娠健康,但是对胎盘vitD转运和代谢的影响以及新生儿vitD状态的了解有限。比较目前的标准产妇补充剂,10微克/天服用90微克维生素D补充剂,我们调查了胎盘基因表达,产妇vitD转运和新生儿vitD状态。从第11-16周开始,从随机分配给10µg或90µgvitD补充剂的孕妇获得生物材料。母体暴露之间可能存在关联,新生儿vitD状态和胎盘vitD受体(VDR)的表达,运输商(Cubilin,CUBN和Megalin,研究了LRP2)和vitD激活和降解酶(CYP24A1,CYP27B1)。补充前后测定母体vitD结合蛋白(VDBP)。总的来说,10µgvitD组中51%的新生儿缺乏vitD,而90µg组中为11%。高剂量vitD补充没有显著影响VDBP或胎盘基因表达。然而,描述性分析表明,母亲肥胖可能导致CUBN的差异表达,CYP24A1和CYP27B1一转变VDBP反响。高剂量vitD改善新生儿vitD状态而不影响胎盘vitD调节。
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