School of Human Sciences, The University of Western Australia, Australia.
Metabolomics Australia, Centre for Microscopy, Characterisation and Analysis, The University of Western Australia, Australia.
Placenta. 2019 Aug;83:5-7. doi: 10.1016/j.placenta.2019.06.001. Epub 2019 Jun 4.
Maternal vitamin D deficiency disturbs fetal development and programmes neurodevelopmental complications in offspring, possibly through increased fetal glucocorticoid exposure. We aimed to determine whether prenatal exposure to excess glucocorticoids underlies our rat model of early-life vitamin D deficiency, leading to altered adult behaviours. Vitamin D deficiency reduced the expression of the glucocorticoid-inactivating enzyme Hsd11b2 in the female placenta, but did not alter maternal glucocorticoid levels, feto-placental weights, or placental expression of other glucocorticoid-related genes at mid-gestation. This differs to the phenotype previously observed in vitamin D deficient mice, and highlights important modelling considerations.
母体维生素 D 缺乏会干扰胎儿的发育，并使后代出现神经发育并发症，这可能是通过增加胎儿糖皮质激素暴露所致。我们旨在确定在我们的早期生活维生素 D 缺乏大鼠模型中，是否存在过多的糖皮质激素暴露导致改变成年行为。维生素 D 缺乏会降低雌性胎盘的糖皮质激素失活酶 Hsd11b2 的表达，但不会改变母鼠的糖皮质激素水平、胎-胎盘重量，或胎盘中期表达的其他糖皮质激素相关基因。这与之前在维生素 D 缺乏的小鼠中观察到的表型不同，强调了重要的建模考虑因素。
