In Summary, we demonstrated that PDE could induce hypercholesterolemia susceptibility in adult male offspring rats, and the intrauterine programming mechanism is related to the suppressed expression of fetal hepatocyte LDLR induced by dexamethasone activation of GR through a dual pathway (direct transcriptional inhibition and HDAC2/H3K27ac pathway). The gene discussed is NR3C1; the disease is familial hypercholesterolemia.