Abstract
As the major cause of female anovulatory infertility, polycystic ovary syndrome (PCOS) affects a great proportion of women at childbearing age. Although glucagon-like peptide 1 receptor agonists (GLP-IRAs) show therapeutic effects for PCOS, its target and underlying mechanism remains elusive. In the present study, we identified that, both in vivo and in vitro, GLP-1 functioned as the regulator of proliferation and antiapoptosis of MGCs of follicle in PCOS mouse ovary. Furthermore, forkhead box protein O1 (FoxO1) plays an important role in the courses. Regarding the importance of granulosa cells (GCs) in oocyte development and function, the results from the current study could provide a more detailed illustration on the already known beneficial effects of GLP-1RAs on PCOS and support the future efforts to develop more efficient GLP-1RAs for PCOS treatment.
Highlights
Polycystic ovary syndrome (PCOS) is diagnosed in 6%–8% of women at childbearing age [1]. e manifestations of PCOS generally include oligomenorrhea or amenorrhea, abnormal folliculogenesis, chronic anovulation, hyperandrogenemia, and infertility [2]
A mouse model of PCOS was established by injecting dehydroepiandrosterone (DHEA) to explore the Glucagon-like peptide 1 (GLP-1)/ GLP-1 receptor (GLP-1R) signal in PCOS ovaries. e results of continuous vaginal smear monitoring showed that all mice in the vehicle group had a regular estrous cycle of 4 to 5 days
In agreement with the metabolic disorder frequently observed in PCOS, the fasting insulin levels in mice with PCOS increased compared with the mice in the vehicle group (P < 0.05) (Figure 1(b))
Summary
Polycystic ovary syndrome (PCOS) is diagnosed in 6%–8% of women at childbearing age [1]. e manifestations of PCOS generally include oligomenorrhea or amenorrhea, abnormal folliculogenesis, chronic anovulation, hyperandrogenemia, and infertility [2]. E complex pathogenesis of PCOS includes abnormal expression of apoptosis correlated genes, MAPK signaling pathway, and cell cycle associated molecules [4]. The proliferation and apoptosis of GCs are the fundamental causes of follicular development and atresia [5]. Taken these together, the study of PCOS GCs is helpful to investigate its physiological and pathological roles during disease progression and further possible pathogenesis. In addition to the effects of GLP-1/GLP-1R axis on metabolism, GLP-1R agonists (GLP-1RAs, such as liraglutide) improved the markers of ovarian function (bleeding pattern; levels of AMH (Anti-Mullerian hormone)), sex hormones, gonadotropins, and ovarian morphology in overweight women with PCOS [9].
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