Neither HF IU nor fetal genotype altered expression of nuclear receptor subfamily 3, group C, member 1 (glucocorticoid receptor, NR3C1) or the critical enzymes that catalyze cortisol metabolism (hydroxysteroid- 11-beta dehydrogenase 1-HSD11B1 and hydroxysteroid- 11-beta dehydrogenase 2-HSD11B2) (Table 3) suggesting that corticosteroid excess is not the mechanism associated with DOHaD in our model [29]. This evidence concerns the gene HSD11B2 and hydrops fetalis.