Abstract
Hyperandrogenism is a key pathologic characteristic of polycystic ovarian syndrome (PCOS), and exercise can alleviate the accompanying inflammation and decrease the high androgen levels, but the mechanism is still unclear, so the purpose of this study is to explore the pathophysiologic characteristics of hyperandrogenic PCOS and the mechanism underlying its amelioration with aerobic exercise. Thirty-two female rats were randomly allocated to a normal control group (NC, n = 8), exercise control group (EC, n = 8), PCOS group (PC, n = 8), and PCOS plus exercise group (PE, n = 8). The PC and PE groups were injected with a dehydroepiandrosterone (DHEA) solution to induce the hyperandrogenic PCOS rat model. The EC and PE groups underwent a Masashi swimming protocol (120 min per session, 6 days/week, for 15 days). Results indicated that the concentrations of leptin (LP) in the EC group were significantly lower than those in the NC group (p < 0.05). Compared with the NC group, the levels of testosterone (T), estradiol (E2), follicle-stimulating hormone (FSH), LP, anti-Müllerian hormone (AMH), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and free fatty acids (FFA) were all significantly augmented in the PC group (all p < 0.05). In addition, compared with the NC group, the levels of adiponectin (ADP) were significantly decreased (p < 0.05), and the expression of aromatase cytochrome P450 (P450arom) in ovarian tissue was significantly elevated in the PC group (p < 0.05). The levels of T, FSH, LP, and FFA were also significantly increased in the PE group (p < 0.05). Compared with the PC group, the levels of T and LP in the PE group were significantly diminished (p < 0.05), and the levels of ADP were significantly increased in the PE group (p < 0.05). T was positively correlated with E2, FSH, AMH, LP, TNF-α, IL-6, and FFA levels, while ADP was negatively correlated with LP and E2. These results showed that hyperandrogenism, chronic low-grade inflammation, and leptin resistance may interact to influence the occurrence and development of PCOS. Aerobic exercise can alleviate the internal inflammation by relieving leptin resistance and may mitigate the sex hormone disorder and hyperandrogenism in rats with PCOS by affecting the hypothalamic-pituitary-ovarian axis.
Highlights
Polycystic ovary syndrome (PCOS) is a common endocrine and metabolic disorder with a global prevalence of 4–21% [1, 2]. e clinical manifestations of PCOS include ovulation failure, menstrual disorders, polycystic ovaries, obesity, and hyperandrogenism associated with hirsutism, acne, and alopecia [3, 4]. e pathogenesis of PCOS still remains unclear, recent studies suggest that it is related to genetic, epigenetic, and environmental factors [5]. e hypothalamic-pituitary-gonadal (HPG) axis regulates the normal gonadal function through the feedback mechanism, and patients with PCOS usually have obvious dysfunction of the hypothalamic-pituitary-ovarian (HPO) axis [6]
PCOS is considered to be associated with chronic low-grade inflammation and increased androgen levels, and these changes can lead to adipocyte hypertrophy [10]. is in turn releases various adipocytokines involved in the regulation of lipid metabolism, inflammation, and reproductive processes [11], resulting in increased serum inflammatory markers such as tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and C-reactive protein (CRP) [12]. ese upregulated markers precipitate chronic low-grade inflammation and lead to a series of sex hormone disorders
Rats in the PC and PE groups were in constant diestrus (Figure 1(d)), and the vaginal smears were predominately composed of neutrophils that were mixed with a few epithelial cells. is successfully validated the PCOS rat model
Summary
Polycystic ovary syndrome (PCOS) is a common endocrine and metabolic disorder with a global prevalence of 4–21% [1, 2]. e clinical manifestations of PCOS include ovulation failure, menstrual disorders, polycystic ovaries, obesity, and hyperandrogenism associated with hirsutism, acne, and alopecia [3, 4]. e pathogenesis of PCOS still remains unclear, recent studies suggest that it is related to genetic, epigenetic, and environmental factors [5]. e hypothalamic-pituitary-gonadal (HPG) axis regulates the normal gonadal function through the feedback mechanism, and patients with PCOS usually have obvious dysfunction of the hypothalamic-pituitary-ovarian (HPO) axis [6]. A relatively low level of FSH and International Journal of Endocrinology development and maturation disorders of the follicle eventually leads to anovulation, polycystic change of the ovarian. PCOS is considered to be associated with chronic low-grade inflammation and increased androgen levels, and these changes can lead to adipocyte hypertrophy [10]. Ese upregulated markers precipitate chronic low-grade inflammation and lead to a series of sex hormone disorders. Other researchers found that due to obesity in PCOS patients, the increased circulating leptin (LP) levels within the body led to leptin resistance, which can significantly promote chronic low-grade inflammation [13]. We speculated that in the pathophysiologic process of PCOS, hyperandrogenism, leptin resistance, and chronic low-grade inflammation may form a vicious cycle, but the relationships among the three are not completely clear
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