Maternal vitamin D deficiency during rat gestation elicits a milder phenotype compared to the mouse model: Implications for the placental glucocorticoid barrier

Rachael C Crew; Ana Rakonjac; Dijana Tesic; Michael W Clarke; Nathanael J Yates; Caitlin S Wyrwoll

doi:10.1016/j.placenta.2019.06.001

Maternal vitamin D deficiency during rat gestation elicits a milder phenotype compared to the mouse model: Implications for the placental glucocorticoid barrier

Placenta. 2019 Aug:83:5-7. doi: 10.1016/j.placenta.2019.06.001. Epub 2019 Jun 4.

Authors

Rachael C Crew¹, Ana Rakonjac¹, Dijana Tesic¹, Michael W Clarke², Nathanael J Yates³, Caitlin S Wyrwoll⁴

Affiliations

¹ School of Human Sciences, The University of Western Australia, Australia.
² Metabolomics Australia, Centre for Microscopy, Characterisation and Analysis, The University of Western Australia, Australia.
³ School of Human Sciences, The University of Western Australia, Australia; Asia-Pacific Centre for Neuromodulation, Queensland Brain Institute, University of Queensland, Australia.
⁴ School of Human Sciences, The University of Western Australia, Australia. Electronic address: caitlin.wyrwoll@uwa.edu.au.

PMID: 31477207
DOI: 10.1016/j.placenta.2019.06.001

Abstract

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.

Keywords: Glucocorticoids; Placenta; Vitamin D.

Publication types

Comparative Study
Research Support, Non-U.S. Gov't

MeSH terms

11-beta-Hydroxysteroid Dehydrogenase Type 2
Animals
Disease Models, Animal
Female
Gene Expression
Glucocorticoids / metabolism*
Male
Maternal-Fetal Exchange
Mice
Mice, Inbred BALB C
Phenotype
Placenta / metabolism*
Pregnancy
Pregnancy Complications / genetics
Pregnancy Complications / metabolism*
Prenatal Exposure Delayed Effects / metabolism
Rats
Rats, Sprague-Dawley
Species Specificity
Vitamin D Deficiency / complications*
Vitamin D Deficiency / genetics
Vitamin D Deficiency / metabolism*

Substances

Glucocorticoids
11-beta-Hydroxysteroid Dehydrogenase Type 2