Abstract
Objectives: Polycystic ovarian syndrome (PCOS) is one of the most prevalent endocrine abnormalities among women in reproductive ages, but the pathogenesis of PCOS is not fully understood. The aim of this study was to establish a PCOS rat model with Recombinant Human insulin growth factor-1 (RH-IGF-1), we assessment the characteristics of hyperinsulinemia and hyperandrogenism in this rat model. Methods: Rats were randomly divided into two groups. The rats were treated with RH-IGF-1 2mg/100g daily in RHIGF-1 group(n=20), and in the saline group (n =14) rats were treated with 0.9% Sodium Chloride 0.2ml/100g daily. The experiment was carried out in two stages, in Stage I, rats were anesthetized after complete the first estrous cycle in the saline group, tissue and blood samples were collected(n=7), and in the RH-IGF-1 treated group the rats were anesthetized at the 5th day after VO (n=10). In Stage II, in the saline group rats were anesthetized after three complete cycles(n=7), meanwhile, rats were anesthetized in the RH-IGF-1 group at the 15th day after VO(n=10). Results: We found that the rats in RH-IGF-1 group had the characteristics of PCOS, after injected RH-IGF-1, the VO of the rats was significantly earlier, the expression of IGF-1 mRNA and protein in adrenal tissue was increased. Conclusions: These findings suggest that IGF-1 may be a key factor in the pathogenesis of PCOS, the increase of androgen may be the pathological result of polycystic ovary syndrome, not the cause.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.