Abstract
Polycystic ovary syndrome (PCOS) is a common endocrine disorder, affecting 9–18% of women in reproductive age that causes hyperandrogenism and infertility due to dysfunctional follicular maturation and anovulation. The etiology of PCOS is still poorly known, and information from experimental animal models may help improve current understanding of the mechanisms of PCOS initiation and development. Therefore, we conducted a systematic review of currently available methods for simulation of PCOS in experimental models, focusing on two main endocrine traits: ovarian morphology changes and circulating levels of sex hormones and gonadotropins.We searched the MEDLINE database for articles in English or Spanish published until October 2016. Of 933 studies identified, 39 were included in the systematic review. One study compared interventions with androgens versus estrogens, 18 used androgen-induced stimulation, 9 used estrogens or drugs with estrogen action, including endocrine disruptors, to induce PCOS-like models, and 12 used miscellaneous interventions. Broad differences were found among the studies concerning hormonal interventions, animal species, and developmental stage at the time of the experiments, and most models resulted in ovarian morphology changes, mainly increases in the number of cystic and antral follicles and decreases in the corpus luteum. Hyperandrogenism was produced by using androgens and other drugs as the stimulatory agent. However, studies using drugs with estrogenic effect did not observe changes in circulating androgens.In conclusion, medium- or long-term testosterone administration in the pre- and postnatal periods performed best for induction of a PCOS-like phenotype, in rhesus macaque and rat models respectively. In rats, postnatal exposure to androgens results in reprogramming of the hypothalamic-pituitary-ovarian-axis. Thus, comparisons between different intervention models may be useful to define the timing of reproductive PCOS phenotypes in experimental animal models.
Highlights
Polycystic ovary syndrome (PCOS) is one of the most common endocrine conditions, affecting 9–18% of women of reproductive age, depending on diagnostic criteria [1]
PCOS is characterized by at least two of the three following criteria: clinical or biochemical hyperandrogenism, oligo/anovulation, and polycystic ovaries [2]. These manifestations are associated with reduced fertility, due to dysfunctional follicular maturation and consequent anovulation, and hyperandrogenism, causing acne and hirsutism [3]. Both chronic anovulation and androgen excess are linked to disturbed folliculogenesis, that is expressed by multiple cystic follicles between 2 and 9 mm and increased ovarian volume in women with PCOS [4]
39 studies were included in the systematic review: 19 animal models using androgen-induced stimulation [10,11,12,13,14,15,16,17,18,19,20,21,22,23,24,25,26,27,28]; 9 which employed estrogens and estrogen-like drugs to induce a PCOS-like syndrome [27, 29,30,31,32,33,34,35,36]; and 12 using other interventions [37,38,39,40,41,42,43,44,45,46,47,48]
Summary
Polycystic ovary syndrome (PCOS) is one of the most common endocrine conditions, affecting 9–18% of women of reproductive age, depending on diagnostic criteria [1]. PCOS is characterized by at least two of the three following criteria: clinical or biochemical hyperandrogenism, oligo/anovulation, and polycystic ovaries [2] These manifestations are associated with reduced fertility, due to dysfunctional follicular maturation and consequent anovulation, and hyperandrogenism, causing acne and hirsutism [3]. Clinical studies have suggested that girls with PCOS exhibit increased gonadotropin releasing hormone (GnRH) pulse frequency, leading to excess luteinizing hormone (LH) secretion This causes premature acquisition of LH receptor expression by growing ovarian follicles at excessively early stages, leading to increased ovarian androgen production [6, 7] and, probably, to the arrested antral follicle development of PCOS [8]. PCOS-affected ovaries exhibit an increase in the number of growing preantral and antral follicles, which leads to antrum expansion, increased granulosa cell degeneration, and development of cystic follicles, with thin granulosa cell walls and a thicker surrounding layer of theca cells [8]
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