scholarly journals Expression and Contribution of Insulin Signaling Pathway to the Development of Polycystic Ovary Syndrome

2020 ◽  
Author(s):  
Qingqiang Lin ◽  
Hong Zhang ◽  
Jiuhua Zhao ◽  
Zhengchao Wang
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Signaling Pathway ◽  
Insulin Signaling ◽  
Polycystic Ovary ◽  
Insulin Signaling Pathway ◽  
Ovary Syndrome

scholarly journals Local Cortisol Elevation Contributes to Endometrial Insulin Resistance in Polycystic Ovary Syndrome

2018 ◽  
Vol 103 (7) ◽  
pp. 2457-2467 ◽  
Author(s):  
Jia Qi ◽  
Wangsheng Wang ◽  
Qinling Zhu ◽  
Yaqiong He ◽  
Yao Lu ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Polycystic Ovary Syndrome ◽  
Glucose Uptake ◽  
Signaling Pathway ◽  
Insulin Signaling ◽  
Glucose Transporter ◽  
Polycystic Ovary ◽  
Implantation Rate ◽  
Insulin Signaling Pathway ◽  
Ovary Syndrome

Abstract Context Endometrial insulin resistance (IR) may account for the endometrial dysfunction in polycystic ovary syndrome (PCOS). The underlying mechanism remains to be elucidated. Objective To investigate whether the abundance of 11β-hydroxysteroid dehydrogenases (11β-HSDs) 1 and 2 and cortisol as well as the insulin signaling pathway are altered in PCOS endometrium and to clarify the relationship between endometrial IR and local cortisol. Design We measured cortisol and cortisone concentrations, 11β-HSD1 and 11β-HSD2, and core insulin signaling molecules in endometrial biopsies collected from non-PCOS and PCOS with or without IR patients on the seventh day after human chorionic gonadotropin injection. We also studied the effects of cortisol on glucose uptake and the insulin signaling pathway in primary cultured endometrial epithelial cells (EECs). Results The cortisol concentration was elevated, whereas 11β-HSD2 expression was diminished in endometrial biopsies obtained from PCOS with IR patients compared with those from non-PCOS and PCOS without IR patients. The implantation rate was relatively impaired and the endometrial insulin signaling pathway was defective in PCOS with IR patients. In addition, cortisol attenuated insulin-stimulated glucose uptake in EECs, which was mediated by inhibition of Akt phosphorylation and glucose transporter type 4 translocation via induction of phosphatase and tensin homolog deleted on chromosome ten (PTEN). Conclusions Decreased oxidation of cortisol and defects of insulin signaling in endometrium were observed in PCOS with IR patients. The excessive cortisol level, derived from the reduction of 11β-HSD2, might contribute to the development of endometrial IR by inhibiting the insulin signaling pathway via induction of PTEN expression in EECs.

scholarly journals Changes in the Expression of Insulin Signaling Pathway Molecules in Endometria from Polycystic Ovary Syndrome Women with or without Hyperinsulinemia

2009 ◽  
Vol 16 (3-4) ◽  
pp. 129-136 ◽  
Author(s):  
Romina Fornes ◽  
Paulina Ormazabal ◽  
Carlos Rosas ◽  
Fernando Gabler ◽  
David Vantman ◽  
...  
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Signaling Pathway ◽  
Insulin Signaling ◽  
Polycystic Ovary ◽  
Insulin Signaling Pathway ◽  
Ovary Syndrome

scholarly journals The role of serum inflammatory cytokines and berberine in the insulin signaling pathway among women with polycystic ovary syndrome

PLoS ONE ◽  
2020 ◽  
Vol 15 (8) ◽  
pp. e0235404 ◽  
Author(s):  
Hongying Kuang ◽  
Yuwei Duan ◽  
Dan Li ◽  
Yanwen Xu ◽  
Wenxia Ai ◽  
...  
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Signaling Pathway ◽  
Inflammatory Cytokines ◽  
Insulin Signaling ◽  
Polycystic Ovary ◽  
Insulin Signaling Pathway ◽  
Ovary Syndrome

Notch signaling pathway in cumulus cells reflecting zygote and embryo quality in polycystic ovary syndrome

2021 ◽  
Author(s):  
Mojtaba Masoudi ◽  
Nazila Yamini ◽  
Fahimeh Salehi ◽  
Reza Aflatoonian ◽  
Maryam Azizi Kutenaee ◽  
...  
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Notch Signaling ◽  
Signaling Pathway ◽  
Embryo Quality ◽  
Polycystic Ovary ◽  
Cumulus Cells ◽  
Notch Signaling Pathway ◽  
Ovary Syndrome

scholarly journals Adiponectin Reduces Embryonic Loss Rate and Ameliorates Trophoblast Apoptosis in Early Pregnancy of Mice with Polycystic Ovary Syndrome by Affecting the AMPK/PI3K/Akt/FoxO3a Signaling Pathway

2020 ◽  
Vol 27 (12) ◽  
pp. 2232-2241 ◽  
Author(s):  
Wenqian Zhang ◽  
Meng Zuo ◽  
Juan Lu ◽  
Yuxia Wang
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Signaling Pathway ◽  
Early Pregnancy ◽  
Loss Rate ◽  
Polycystic Ovary ◽  
Uterine Tissue ◽  
Trophoblast Cells ◽  
Ovary Syndrome ◽  
Villous Trophoblast ◽  
Embryo Loss

Abstract Reports in recent years have suggested that adiponectin (APN) improves insulin resistance and inhibits apoptosis by activating the AMP-activated protein kinase (AMPK) pathway and the PI3K/Akt signaling pathway after binding to its receptor. This study aims to explore the mechanism by which APN reduces embryo loss rate and trophoblast apoptosis in early pregnancy of mice with polycystic ovary syndrome (PCOS). PCOS mice were subcutaneously injected with APN (10 μg mg kg−1 day−1) on 11 consecutive days from the 3rd day of pregnancy onwards to observe the change of the embryo loss rate of PCOS mice induced by APN. Quantitative real-time PCR and Western blot were used to determine the relative expressions of mRNA and the proteins AMPK, PI3K, and Akt in mouse uterine tissue. At the same time, primary cultured mouse villous trophoblast cells were used to further explore the underlying mechanisms in vitro. APN significantly reduces the pregnancy loss rate of PCOS mice. At the same time, APN increases phosphorylation and mRNA expression levels of AMPK, PI3K, and Akt in PCOS mouse uterine tissue. In addition, trophoblast cells of model mice were treated with APN and inhibitors, and APN was found to reduce trophoblast cell apoptosis by affecting the phosphorylation levels of AMPK, PI3K, Akt, and FoxO3a proteins. APN reduces the embryo loss rate and ameliorates trophoblast apoptosis in PCOS mice by affecting the AMPK/PI3K/AKT/FoxO3a signaling pathway.

Defects in insulin signaling pathways in ovarian steroidogenesis and other tissues in polycystic ovary syndrome (PCOS)

2008 ◽  
Vol 109 (3-5) ◽  
pp. 242-246 ◽  
Author(s):  
Evanthia Diamanti-Kandarakis ◽  
Georgia Argyrakopoulou ◽  
Frangiskos Economou ◽  
Eleni Kandaraki ◽  
Michael Koutsilieris
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Signaling Pathways ◽  
Insulin Signaling ◽  
Polycystic Ovary ◽  
Ovary Syndrome ◽  
Ovarian Steroidogenesis

Polymorphism in postinsulin receptor signaling pathway is not associated with polycystic ovary syndrome

2008 ◽  
Vol 90 (6) ◽  
pp. 2298-2303 ◽  
Author(s):  
Michelle R. Jones ◽  
Scott G. Wilson ◽  
Ben H. Mullin ◽  
Robert Mead ◽  
Frank Dudbridge ◽  
...  
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Signaling Pathway ◽  
Polycystic Ovary ◽  
Receptor Signaling ◽  
Ovary Syndrome ◽  
Receptor Signaling Pathway
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