Prenatal dexamethasone exposure programs the decreased testosterone synthesis in offspring rats by low level of endogenous glucocorticoids.

ABSTRACT: Prenatal dexamethasone exposure (PDE) can decrease maternal endogenous glucocorticoid level and induce testicular dysplasia in male offspring rats. In this study we investigated low level endogenous glucocorticoid-mediated testicular dysplasia in PDE offspring and elucidated the intrauterine epigenetic programming mechanisms. Pregnant rats were injected with dexamethasone (0.2 mg·kg^-1·d^-1, sc) on gestational day (GD) 9-20. The offspring rat blood and testis were collected after euthanasia on GD20, postnatal week (PW) 12 or PW28. We showed that PDE induced abnormal morphology of testis and significantly decreased the expression of testosterone synthesis-related genes as well as testosterone production before and after birth. Meanwhile, serum corticosterone, the express

SUBMITTER: Liu M 

PROVIDER: S-EPMC9159998 | biostudies-literature | 2022 Jun

REPOSITORIES: biostudies-literature