ArticlePloS one2018
Antenatal exposure to betamethasone induces placental 11β-hydroxysteroid dehydrogenase type 2 expression and the adult metabolic disorders in mice.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 9 citations in OpenAlex.
- Sex-specific effects of betamethasone on glucocorticoid and apoptotic signalling pathways in the sheep placenta.The Journal of physiology · 2025Article
- The effect of time interval between antenatal corticosteroid administration and delivery on outcomes in late preterm neonates born to mothers with diabetes: a retrospective cohort study.Frontiers in pediatrics · 2023Article
- Effects of Maternal Chewing on Prenatal Stress-Induced Cognitive Impairments in the Offspring via Multiple Molecular Pathways.International journal of molecular sciences · 2020Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Antenatal overexposure to glucocorticoids causes fetal intrauterine growth restriction (IUGR) and adult metabolic disorders. 11β-hydroxysteroid dehydrogenase (11β-HSD) 1 and 2 are key enzymes for glucocorticoid metabolism, however, the detailed effects of antenatal overexposure to glucocorticoids on placental 11β-HSD1 and 2 expression and adult metabolic disorders remain obscure. Here, we report that, in placenta 11β-HSD1 is diffusely localized, whereas 11β-HSD2 is specifically expressed in labyrinthine layer. Exposure of pregnant dams to betamethasone significantly increases the expression of placental 11β-HSD2 but not 11β-HSD1, and decreases the weights of fetuses but not placentas. Antenatal exposure to betamethasone leads to either significant weight loss in the offspring younger than 10-week-old, or weight gain in those older than 14-week-old. Furthermore, antenatal exposure to betamethasone results in coexistence of various metabolic disorders in adult offspring, including hyperglycemia, glucose intolerance, low insulin secretory capacity and hyperlipidemia. The present study demonstrates that exposure of pregnant dams to betamethasone induces the expression of placental 11β-HSD2 but not 11β-HSD1, leads to fetal IUGR and causes adult metabolic disorders, providing evidence for fetal origins of adult diseases and the potential role of placental 11β-HSD2 in them.
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