Congenital Adrenal Hyperplasia Insights

In their study, Cao et al. (2025) found that prenatal dexamethasone exposure (PDE) can lead to adrenal dysfunction in adult male offspring. This is due to an increase in the acetylation levels and expression of the enzyme CYP27A1, which is involved in bile acid production in the adrenal gland. The study showed that this increase in CYP27A1 leads to higher bile acid levels, causing stress to the endoplasmic reticulum (a cell structure where proteins are made) and impairing cell function.

Interestingly, the effects of PDE were reversed in female offspring. The researchers also discovered that treating male offspring with nilvadipine, a CYP27A1 inhibitor, after birth could reverse the morphological and functional damage to the adrenal gland caused by PDE. These findings suggest that the GR/SETBP1 signaling pathway plays a crucial role in the PDE-induced adrenal dysfunction observed in adult male offspring.