Tingting He1, Yuan Liu2, Shigang Zhao1, Hongbin Liu3, Ze Wang1, Yuhua Shi4. 1. Center for Reproductive Medicine, Shandong University, China; National Research Center for Assisted Reproductive Technology and Reproductive Genetics, China; The Key Laboratory of Reproductive Endocrinology (Shandong University), Ministry of Education, China; Shandong Provincial Clinical Medicine Research Center for Reproductive Health, Jinan, 250100, China. 2. Department of OB&GYN, Qilu Hospital of Shandong University, Jinan, 250012, China. 3. Center for Reproductive Medicine, Shandong University, China; National Research Center for Assisted Reproductive Technology and Reproductive Genetics, China; The Key Laboratory of Reproductive Endocrinology (Shandong University), Ministry of Education, China; Shandong Provincial Clinical Medicine Research Center for Reproductive Health, Jinan, 250100, China; CUHK-SDU Joint Laboratory on Reproductive Genetics, School of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong, China. 4. Center for Reproductive Medicine, Shandong University, China; National Research Center for Assisted Reproductive Technology and Reproductive Genetics, China; The Key Laboratory of Reproductive Endocrinology (Shandong University), Ministry of Education, China; Shandong Provincial Clinical Medicine Research Center for Reproductive Health, Jinan, 250100, China. Electronic address: shiyuhua2003@126.com.
Abstract
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). 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 PCOSpatients 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 PCOSpatients (p < 0.05). 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.