, Volume 53, Issue 3, pp 823–830 | Cite as

Metabolic actions of insulin in ovarian granulosa cells were unaffected by hyperandrogenism

  • Shidou Zhao
  • Haijing Xu
  • Yuqian Cui
  • Wenting Wang
  • Yingying Qin
  • Li You
  • Wai-Yee Chan
  • Yun Sun
  • Zi-Jiang ChenEmail author
Original Article


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, insulin-induced 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.


High androgen Granulosa cell Insulin resistance Polycystic ovary syndrome 



This work was supported by the National Basic Research Program of China (973 program, 2012CB944700); National Natural Science Foundation of China (81200419); Shandong Province Excellent Young and Middle-Aged Scientists Research Awards Fund (BS2013YY012); Key Program for Basic Research of the Science and Technology Commission of Shanghai Municipality, China (12JC1405800); China Postdoctoral Science Foundation Funded Project (2012M511522, 2013T60677); and Postdoctoral Innovation Foundation of Shandong Province (201203043). The authors thank all of their colleagues for technical support.

Compliance with ethical standards

Conflict of interest

All of the authors have no conflict of interest to declare.

Supplementary material

12020_2016_949_MOESM1_ESM.pdf (386 kb)
Supplementary material 1 (PDF 385 kb)


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Copyright information

© Springer Science+Business Media New York 2016

Authors and Affiliations

  • Shidou Zhao
    • 1
    • 2
  • Haijing Xu
    • 3
  • Yuqian Cui
    • 1
  • Wenting Wang
    • 1
  • Yingying Qin
    • 1
  • Li You
    • 1
  • Wai-Yee Chan
    • 2
  • Yun Sun
    • 3
  • Zi-Jiang Chen
    • 1
    • 3
    Email author
  1. 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 EducationShandong Provincial Key Laboratory of Reproductive MedicineJinanPeople’s Republic of China
  2. 2.The Chinese University of Hong Kong-Shandong University Joint Laboratory on Reproductive Genetics, School of Biomedical SciencesThe Chinese University of Hong KongShatinChina
  3. 3.Shanghai Key Laboratory for Assisted Reproduction and Reproductive Genetics, Center for Reproductive Medicine, Renji Hospital, School of MedicineShanghai Jiao Tong UniversityShanghaiPeople’s Republic of China

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