ESPEYB19 14. Science and Medicine Steroidogenesis and beyond (4 abstracts)
14.7. Placental uptake and metabolism of 25(OH)vitamin D determine its activity within the fetoplacental unit
Ashley B , Simner C , Manousopoulou A , Jenkinson C , Hey F , Frost JM , Rezwan FI , White CH , Lofthouse EM , Hyde E , Cooke LDF , Barton S , Mahon P , Curtis EM , Moon RJ , Crozier SR , Inskip HM , Godfrey KM , Holloway JW , Cooper C , Jones KS , Lewis RM , Hewison M , Garbis SDD , Branco MR , Harvey NC & Cleal JK
The Institute of Developmental Sciences, Human Development and Health, Faculty of Medicine University of Southampton, Southampton, United Kingdom
eLife 2022;11:e71094 doi: 10.7554/eLife.71094
Brief summary: Using placental perfusion, placental fragment culture and primary term human cytotrophoblast culture experiments, the authors signify the relationship between maternal vitamin D, placental vitamin D metabolism and fetal vitamin D exposure.
In this study, the uptake of radio-labelled vitamin D (13C-25(OH)D3) could be elegantly traced from the maternal unit to the placental unit through to the fetal compartment, with the placental unit additionally metabolising and storing maternal vitamin D. Active placental metabolism of maternal vitamin D resulted in the biosynthesis of downstream C24- and C1-hydroxylated vitamin D metabolites, both of which were released into the maternal and fetal compartments, while these metabolites also remained within the placental pool. Of the two downstream metabolites, C24-hydroxylated vitamin D was predominantly produced in the placenta and two-fold more of this metabolite was released into the maternal unit compared to the fetal compartment, also supported by positive correlations between placental and maternal vitamin D metabolite levels.
Importantly, the authors show that vitamin D uptake is an active uptake mechanism- not by simple diffusion – entailing similar mechanisms of endocytosis as observed in the kidney. This study furthermore shows that exposure of the placenta to vitamin D leads to transcriptomic and proteomic changes in the placenta, which ultimately impact the specificity of the vitamin D response in the fetal-placental unit. Bringing these results into context of the fetus, these findings predict that impaired placental transport and metabolism of maternal vitamin D may hinder fetal development. Indeed, the authors substantiate their conclusions with results from a cohort study, in which placental expression levels of key vitamin D metabolising enzymes and metabolic genes were associated with fetal size measurements.
This is the first quantitative study to demonstrate vitamin D transfer and (most importantly) metabolism by the human placenta. It reveals a complex interplay between vitamin D and the placenta, with ultimate impact on fetal growth and development. These results are important and now the continuing story of the cooperation between vitamin D and the fetal-placental unit needs to be understood within the context of early gestation to fully understand the translational capacity of these results.
Volume 19
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ESPE Yearbook of Paediatric Endocrinology
ISSN 1662-4009 (Online)
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