Animal models of the polycystic ovary syndrome phenotype

Abstract

The etiology of the polycystic ovary syndrome (PCOS) remains unclear, despite its high prevalence among infertility disorders in women of reproductive age. Although there is evidence for a genetic component of the disorder, other causes, such as prenatal insults are considered among the potential factors that may contribute to the development of the syndrome. Over the past few decades, several animal models have been developed in an attempt to understand the potential contribution of exposure to excess steroids on the development of this syndrome. The current review summarizes the phenotypes of current animal models exposed to excess steroid during the prenatal and early postnatal period and how they compare with the phenotype seen in women with PCOS.

Prenatal Exposure of Kisspeptin Antagonist on the GonadotropinReleasing Hormone (GnRH) Expression in Rat Model of Polycystic Ovary Syndrome

“…In agreement with our results, previous studies have reported disrupted hormonal profile in PCOS animal models, compared to controls [33]. Evidence for endocrine changes in PCOS animal models is inconsistent, indicating the differences may be due to various factors, including type of hormone administered, time of hormone exposure, age of animal during the time of study, different PCOS phenotypes in animal models and time of sampling [21,[33][34][35].…”

“…These animals exhibit elevated LH pulse frequency and irregular reproductive cycles, which may result from a number of mechanisms, including alterations in synaptic input to GnRH neurons, 2004, desensitization of GnRH neurons to steroid feedback, increased amplitude/frequency of GnRH pulses, and increased gonadotropic sensitivity to the GnRH stimulation [20][21][22][23][24]. Kisspeptin, an essential gatekeeper of puberty onset and GnRH secretion, mediates steroid feedback and metabolic cues during different developmental stages throughout the lifespan [9,25].…”

MicroRNA in Ovarian Biology and Disease

“…For instance, prenatal exposure to testosterone is known to cause polycystic ovarian syndrome (PCOS) in adult females as evidenced by increased follicle recruitment, disrupted cyclicity, and high estradiol secretion (Padmanabhan and Veiga-Lopez 2013). When pregnant ewes were exposed to high levels of androgens beginning at day 30 of gestation, the female offspring develop a PCOS phenotype as adults.…”

Efeitos do exercício sobre os aspectos metabólicos e reprodutivos de modelos murinos de síndrome dos ovários policísticos

“…Pode-se induzir o aparecimento de fenótipos similares à SOP com exposição a esteroides sexuais (22,23), letrozol (24), luz contínua (25), entre outros (26). Espécies tais como primatas, ovelhas, ratos e camundongos tem sido utilizados como modelos animais de SOP (27). Porém, o uso de primatas e ovelhas para pesquisa é extremamente caro (22,28).…”

“…Diversos estudos tem utilizado a exposição a esteroides sexuais no período pré-natal, neonatal ou pré-puberal (27). Em ratas, foi mostrado que a exposição pré-puberal à dihidrotestosterona (DHT), que é um androgênio não aromatizável, induz a características metabólicas e reprodutivas similares à SOP na vida adulta desses animais (22 Há diversas diferenças fisiológicas dos adipócitos subcutâneos para os viscerais, especialmente em transporte e armazenamento de ácidos graxos, lipólise, produção de adipocinas e adaptação ao balanço energético positivo e negativo (36).…”