The low-expression programming of 11β-HSD2 mediates osteoporosis susceptibility induced by prenatal caffeine exposure in male offspring rats.

ABSTRACT:

Background and purpose

Prenatal caffeine exposure (PCE) can cause developmental toxicity of long bones in offspring, but the long-term effects and the underlying mechanism have not been fully clarified. Here, we investigated the effects of PCE peak bone mass accumulation and osteoporosis susceptibility in offspring and its intrauterine programming mechanism.

Experimental approach

Pregnant Wistar rats were administrated intragastrically with saline or caffeine (120 mg·kg^-1 ·day^-1 ) on gestational days 9-20. The serum and bone samples were collected from the fetal and postnatal offspring for bone mass, genes expression and corticosterone analysis. Then, rat bone marrow mesenchymal stem cells (BMSCs) were treated with corticosterone in vitro to confirm the

SUBMITTER: Xiao H 

PROVIDER: S-EPMC7520449 | biostudies-literature | 2020 Oct

REPOSITORIES: biostudies-literature