Given that fetal adrenal development and maturation occur during late gestation in rats, the aim of this study was to evaluate the expression of proteins and enzymes involved in steroidogenesis and catecholamine synthesis in adrenal glands from IUGR fetuses. A gene microarray was performed to investigate for alteration in the pathways participating in hormone production. Results show that increased aldosterone serum concentrations in IUGR fetuses were associated with higher mRNA adrenal levels of angiotensin II receptor type 1 (AT1R) and cytochrome P450 aldosterone synthase in response to decreased serum sodium content. Conversely, reduced serum corticosterone concentrations in these fetuses appear to result from alterations in gene expression involved in cholesterol metabolism, such as the augmented apolipoprotein E levels, and in steroidogenesis, like the decreased levels of cytochrome P45011-hydroxylase. Furthermore, increased AT2R expression and the presence of hypoxia and oxidative stress may, in turn, explain the higher adrenal mRNA levels of enzymes involved in catecholamine synthesis. Despite this increase, catecholamine adrenal content was reduced in males and was similar in females compared with sex-matched controls, suggesting higher catecholamine secretion. This could be associated with the induction of genes involved in inflammation-related, acute-phase response in IUGR fetuses. All of these alterations could have long-lasting health effects and may, hence, be implicated in the pathogenesis of increased blood pressure and cardiac hypertrophy observed in IUGR adult animals from this model. fetal programming; developmental plasticity; steroidogenesis; catecholamine ASSOCIATION BETWEEN LOW BIRTH weight and the increased risk of cardiovascular and metabolic diseases in adult life has been confirmed by many epidemiological and animal studies (2, 27). These links could be explained by the processes of normal developmental plasticity that can be affected in response to environmental factors during early life. Indeed, fetal adaptations as a response to impaired intrauterine environment lead to fine physiological settings (alterations in tissue anatomy or microanatomy, cellular activity, and gene expression), which, in turn, can be maladaptative to adult life (3, 13). For example, prenatal hypoxia in rats has been reported to delay the maturation of the adrenal medulla, evidenced by the lower percentage of chromaffin cells expressing tyrosine hydroxylase (TH) and phenylethanolamine N-methyl transferase (PNMT) until postnatal day 7, compared with normoxic offspring (23). Interestingly, the decreased TH activity at 10 wk of age suggests that this impaired adrenal function persists until adulthood (23). In sheep, experimental restriction of placental function (removing endometrial caruncles prior to mating) results in growth-restricted fetuses that present an increase in adrenal gland weight associated with higher plasma cortisol (32), likely due to enhanced expression of cholesterol side-chain cleavage cyt...