IMR Press / CEOG / Volume 45 / Issue 2 / DOI: 10.12891/ceog3834.2018

Clinical and Experimental Obstetrics & Gynecology (CEOG) is published by IMR Press from Volume 47 Issue 1 (2020). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with S.O.G.

Original Research
Influence of pretreatment of insulin on phosphorylation of extracellular receptor kinase by gonadotropin releasing hormone in cultured mouse granulosa gells
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1 Department of Obstetrics and Gynecology, University of Ulsan College of Medicine, Asan Medical Center, Seoul, Republic of Korea
Clin. Exp. Obstet. Gynecol. 2018, 45(2), 252–256; https://doi.org/10.12891/ceog3834.2018
Published: 10 April 2018
Abstract

Background: To investigate the influence of pretreatment of insulin on the phosphorylation of extracellular receptor kinase (ERK) by gonadotropin releasing hormone (GnRH) in cultured mouse granulosa cells. Materials and Methods: The granulosa cells from the mouse were collected simultaneously from the ovaries of gonadotropin-primed ICR female mice. Semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) was used to examine the expression of the receptors of GnRH and insulin. The granulosa cells were cultured with ten nM of insulin, ten nM of GnRH, and ten nM of insulin pretreatment before ten nM of GnRH. Western blotting was used for analysis of phosphorylation of ERK. Student t-test and Dunnett’s comparison test were used for statistical analysis and statistical significance was defined as p < 0.05. Results: The authors confirmed the presence of receptors of GnRH and insulin in the mouse granulosa cells by RTPCR. Both insulin and GnRH could activate ERK phosphorylation. Pretreatment of insulin for 30 minutes before GnRH treatment inhibited ERK phosphorylation by GnRH. Conclusion: Insulin might have a negative effect of GnRH regulation of mouse ovarian physiology by inhibition of GnRH activation of ERK. Based on these study results, the authors demonstrated the role of insulin as a delicate modulator of reproductive function.
Keywords
Extracellular receptor kinase
Gonadotropin releasing hormone
Insulin
Mouse granulosa cells
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