The impact of neonatal androgen receptor (AR) stimulation/blockage, due to testosterone propionate (TP)/AR antagonist treatment, on individual anthropometry and neuroendocrine-metabolic function was evaluated in the juvenile female rat. Pups (age 5 days) were s.c. injected with TP (1.25？mg), flutamide (F; 1.75？mg), and TP？+？F or vehicle (control, CT) and studied on day 30 of age. Body weight (BW), parametrial adipose tissue (PMAT) mass, food intake, adipoinsular axis, and steroidogenic functions were examined. Opposite to TP-rats, F-treated rats developed hypophagia, grew slowly (BW and PMAT), and displayed heightened peripheral insulin sensitivity. These F effects were abrogated in TP？+？F animals. Accordingly, TP rats displayed hyperleptinemia, an effect fully prevented by F cotreatment. Finally, androgen-treated animals bore an irreversible ovarian dysfunction (reduced circulating levels of 17HOP4 and ovary 17HOP4 content and P450c17 mRNA abundance). These data indicate that early stimulation of AR enhanced energy store, blockage of AR activity resulted in some beneficial metabolic effects, and neonatally androgenized rats developed a severe ovarian dysfunction. Our study highlights the important role of AR in the early organizational programming of metabolic and neuroendocrine functions. 1. Introduction Intrauterine and early postnatal endogenous and exogenous environments all have an important role for normal metabolic-neuroendocrine functions and neuronal development of the offspring [1]. Fetal sexual differentiation results from complex interplay between genetic and hormonal factors [2, 3], and testosterone playing a key role in these associated events is supported by the fact that excess testosterone in female fetuses results in functional, behavioral, and morphological defects in adulthood [2, 4, 5]. Insulin resistance is frequently associated with hyperandrogenemia, and clinical studies suggest that interaction between insulin and sex hormones takes place in healthy subjects [6]. Moreover, Barraclough CA [7] reported that just a single neonatal s.c. treatment with testosterone propionate (TP) in the female rat produces several metabolic and clinical features of the human polycystic ovary syndrome (PCOS). Moreover, we previously reported that transient androgenization in normal female rats at neonatal [8] or early postpubertal [9] ages did result in a seriously disrupted metabolic phenotype [10] accompanied by impaired peripheral and adipose tissue (AT) insulin sensitivity in adulthood. Since biological active androgens exert their effects
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