In vivo verification of the pathophysiology of lipoid congenital adrenal hyperplasia in the adrenal cortex

Our study showed that the steroidogenic capacity firstly decreased without tissue change (the first hit) and secondarily declined with tissue change (the second hit) in the adrenal cortex of lipoid congenital adrenal hyperplasia. The key feature of the secondary decline of steroidogenic capacity might be the decreased gene expression related to steroid biosynthesis following the lipid accumulation exacerbated by ACTH hypersecretion. Detection of the genes with significant fluctuation in expression between the mice before and 8 wk after TAM induction to regulate STAR expression.