Conclusion
Our findings indicate that IGFIR/PI3K pathway is differently expressed in PCOS GCs compared with controls, with IGFIR, IRS1, IRS2 significantly increased while PTEN decreased. Thus, our study probably provides new evidences about the pathogenesis of PCOS in term of molecular mechanism.
Objective
Polycystic ovary syndrome (PCOS) is the most common multisystem endocrinopathy in women, characterized by chronic hyperandrogenism, ovulatory dysfunction, and polycystic ovaries. But its etiology remains elusive. A plethora of information suggests phosphatidylinositol-3-kinase (PI3K) pathway is key to the pathogenesis of PCOS but little is known about the expression pattern and possible role of insulin like growth factor 1 receptor (IGFIR)/PI3K pathway in PCOS. The goal of this study was to determine whether the core elements of the IGF1R/PI3K pathway were differentially expressed in GCs isolated from PCOS. Study design: Western blot (WB) and reverse transcription-polymerase chain reaction (RT-PCR) for IGF1R, insulin receptor substrate 1 (IRS1), insulin receptor substrate 2 (IRS2) and phosphatase and tensin homolog (PTEN) related to IGFIR/PI3K pathway were performed in GCs isolated from 60 PCOS patients and 60 controls.
Results
Compared to controls, body mass index (BMI), the levels of fasting plasma glucose (FPG), fasting insulin (FINS), anti-Mullerian hormone (AMH), testosterone (T), luteotropic hormone (LH), homeostasis model assessment of insulin resistance (HOMA-IR), antral follicle count (AFC) were markedly elevated while follicle stimulating hormone (FSH) decreased (p < 0.05). Furthermore, at both mRNA and protein levels, the expression of IGF1R, IRS1, IRS2 were significantly increased whereas PTEN was dramatically decreased in PCOS patients (p < 0.05).