Effects of High-Dose Vitamin D Supplementation on Placental Vitamin D Metabolism and Neonatal Vitamin D Status

Author:

Vestergaard Anna Louise12ORCID,Andersen Matilde Kanstrup13ORCID,Andersen Helena Hørdum3ORCID,Bossow Krista Agathe3ORCID,Bor Pinar24,Larsen Agnete3

Affiliation:

1. Department of Obstetrics and Gynaecology, Randers Regional Hospital, 8930 Randers, Denmark

2. Department of Clinical Medicine, Aarhus University, 8200 Aarhus, Denmark

3. Department of Biomedicine, Aarhus University, 8000 Aarhus, Denmark

4. Department of Obstetrics and Gynaecology, Aarhus University Hospital, 8200 Aarhus, Denmark

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.

Funder

Aarhus University

Aase and Ejner Danielsens Foundation

Axel Muusfeldt Foundation

the Augustinus Foundation

the Danish Medical Association Research Foundation

the Toyota Foundation

Director Emil C. Hertz and Wife Inger Hertz’ Foundation

Dagmar Marshall Foundation

the Frimodt-Heineke Foundation

Orkla Care, Denmark

Publisher

MDPI AG

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