Hindawi Publishing Corporation ISRN Endocrinology Volume 2013, Article ID 181950, 7 pages http://dx.doi.org/10.1155/2013/181950 Research Article Impact of Neonatal Manipulation of Androgen Receptor Function on Endocrine-Metabolic Programming in the Juvenile Female Rat Luisina Ongaro, 1 Andres Giovambattista, 1 and Eduardo Spinedi 1,2 1 Neuroendocrine Unit, IMBICE (CICPBA-CONICET La Plata), 1900 La Plata, Argentina 2 CENEXA (UNLP-CONICET La Plata, PAHO/WHO Collaborating Centre for Diabetes), Medical School, La Plata National University, Calles 60 y 120, 1900 La Plata, Argentina Correspondence should be addressed to Eduardo Spinedi; spinedi@cenexa.org Received 23 May 2013; Accepted 28 July 2013 Academic Editors: C.-H. Anderwald, E. Hajduch, M. Hara, R. Rey, and J. A. Rillema Copyright © 2013 Luisina Ongaro et al. Tis is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Te impact of neonatal androgen receptor (AR) stimulation/blockage, due to testosterone propionate (TP)/AR antagonist treat- ment, 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), futamide (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. Tese F efects were abrogated in TP + F animals. Accordingly, TP rats displayed hyperleptinemia, an efect 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). Tese data indicate that early stimulation of AR enhanced energy store, blockage of AR activity resulted in some benefcial metabolic efects, 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 meta- bolic-neuroendocrine functions and neuronal development of the ofspring [1]. Fetal sexual diferentiation 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 morpho- logical 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 efects through binding to androgen receptor (AR) [11], the present study explored whether neonatal manipulation of AR func- tion in normal female rat could alter metabolic and neu- roendocrine functions when individuals reached juvenile age. For this objective, rats were neonatally treated with either testosterone [7], the nonsteroidal anti-AR futamide [12], or both compounds in combination and then studied at 30 days of age.