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Polycystic ovary syndrome (PCOS) is the most common endocrinopathy in women   of reproductive age. It is a heterogenous disorder, with hyperandrogenism,   chronic anovulation and polycystic ovaries as basic characteristics, and   associated metabolic syndrome features. Increased secretion of leptin and   leptin resistance are common consequences of obesity. Leptin is a hormone   with anorexigenic effects in the hypothalamus. Its function in the regulation   of energy intake and consumption is antagonized by glucocorticoids. By   modulating leptin signaling and inflammatory processes in the hypothalamus,   glucocorticoids can contribute to the development of metabolic disturbances   associated with central energy disbalance. The aim of the study was to   examine the relationship between hypothalamic leptin, glucocorticoid and   inflammatory signaling in the development of metabolic disturbances   associated with PCOS. The study was conducted on an animal model of PCOS   generated by a continual, 90-day treatment of female rats with   5α-dihydrotestosterone (DHT). The model exhibited all key reproductive and   metabolic features of the syndrome. mRNA and/or protein levels of the key   components of hypothalamic glucocorticoid, leptin and inflammatory pathways,   presumably contributing to energy disbalance in DHT-treated female rats, were   measured. The results indicated that DHT treatment led to the development of   hyperphagia and hyperleptinemia as metabolic features associated with PCOS.   However, these metabolic disturbances could not be ascribed to changes in   hypothalamic leptin, glucocorticoid or inflammatory signaling pathways in   DHT-treated rats. [Projekat Ministarstva nauke Republike Srbije, br.   III41009

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5α-dihydrotestosterone treatment induces metabolic changes associated with polycystic ovary syndrome without interfering with hypothalamic leptin and glucocorticoid signaling