Metabolic actions of insulin in ovarian granulosa cells were unaffected by hyperandrogenism
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ORIGINAL ARTICLE
Metabolic actions of insulin in ovarian granulosa cells were unaffected by hyperandrogenism Shidou Zhao1,2 • Haijing Xu3 • Yuqian Cui1 • Wenting Wang1 • Yingying Qin1 Li You1 • Wai-Yee Chan2 • Yun Sun3 • Zi-Jiang Chen1,3
•
Received: 19 October 2015 / Accepted: 31 March 2016 Ó Springer Science+Business Media New York 2016
Abstract Polycystic ovary syndrome (PCOS) patients have intra-ovarian hyperandrogenism and granulosa cells (GCs) from PCOS patients have impaired insulin-dependent glucose metabolism and insulin resistance. The purpose of this study is to determine whether excess androgen affects glucose metabolism and induces insulin resistance of GCs. We firstly explored the insulin metabolic signaling pathway and glucose metabolism in cultured GCs. The Akt phosphorylation and lactate production were increased after insulin treatment. Pre-treatment with PI3-K inhibitor attenuated insulin-induced phosphorylation of Akt and lactate accumulation. However, after treating GCs with different concentrations of testosterone for 5 days, insulininduced phosphorylation of Akt and lactate production
showed no significant change comparing with those of control cells. Finally, mRNA expression of insulin signaling mediators including INSR, IRS-1, IRS-2, and GLUT-4 in GCs was also not significantly altered after testosterone treatment. In conclusion, insulin activates PI3-K/Akt signaling pathway and promotes lactate production in ovarian GCs, but high androgen exerted no obvious influence on insulin signaling pathway and metabolic effect in GCs, suggesting that metabolic actions of insulin in ovarian GCs were unaffected by hyperandrogenism directly. Keywords High androgen Granulosa cell Insulin resistance Polycystic ovary syndrome
Introduction Electronic supplementary material The online version of this article (doi:10.1007/s12020-016-0949-y) contains supplementary material, which is available to authorized users. & Zi-Jiang Chen [email protected] 1
Center for Reproductive Medicine, Shandong Provincial Hospital Affiliated to Shandong University, National Research Center for Assisted Reproductive Technology and Reproductive Genetics, The Key Laboratory for Reproductive Endocrinology of Ministry of Education, Shandong Provincial Key Laboratory of Reproductive Medicine, 324 Jingwu Road, Jinan 250021, People’s Republic of China
2
The Chinese University of Hong Kong-Shandong University Joint Laboratory on Reproductive Genetics, School of Biomedical Sciences, The Chinese University of Hong Kong, Shatin, Hong Kong, SAR, China
3
Shanghai Key Laboratory for Assisted Reproduction and Reproductive Genetics, Center for Reproductive Medicine, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, People’s Republic of China
Polycystic ovary syndrome (PCOS) is the most common endocrine disorder in women of reproductive age [1]. Its diagnosis can be made based on the presence of two of the three following criteria: androgen excess, ovulatory dysfunction, or polycystic ovaries [2]. A
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