17β-estradiol induces an interaction between adenosine monophosphate-activated protein kinase and the insulin signaling pathway in 3T3-L1 adipocytes

  • Authors:
    • Ju-Young Kim
    • Kyung-Jin Jo
    • Byung-Joon Kim
    • Haing-Woon Baik
    • Seong-Kyu Lee
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  • Published online on: July 18, 2012     https://doi.org/10.3892/ijmm.2012.1070
  • Pages: 979-985
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Abstract

Estrogen (17β-estradiol) has been implicated in maintaining insulin sensitivity. It is thought to act predominantly through genomic pathways and regulate the expression of various genes via binding to estrogen receptors (ERs)-α and -β. 17β-estradiol has been reported to simultaneously stimulate protein kinase B (Akt) and adenosine monophosphate-activated protein kinase (AMPK) in ex vivo skeletal muscle. Since data regarding the interaction between AMPK and the insulin receptor substrate-1 (IRS-1)/Akt pathway are controversial, the correlation between AMPK activation and insulin signaling remains unclear. In this study, we examined whether 17β-estradiol simultaneously stimulates the activation of AMPK and IRS-1/Akt in 3T3-L1 adipocytes as well as the 17β-estradiol-ER-induced interaction between the AMPK and IRS-1/Akt pathway in 3T3-L1 adipocytes not exposed to insulin. 17β-estradiol (10-7 M) rapidly activated AMPK and IRS-1/Akt in 3T3-L1 adipocytes, while the ER-α/β non-specific antagonist, ICI 182.780 (10 µM), and the AMPK antagonist compound C (20 µM) reversed the estrogen-induced activation of AMPK and tyrosine (Tyr)-IRS-1/Akt in these cells. Moreover, 17β-estradiol increased the expression of the peroxisome proliferator-activated receptor-γ coactivator-1α (PGC1α), adiponectin, uncoupling protein 2 (UCP2) and glucose transporter 4 (GLUT4) genes 24 h after treatment, whereas the ER-α/β non-specific antagonist, ICI 182.780 (10 µM), and the AMPK antagonist compound C (20 µM) reversed the estrogen-induced increase in the expression of these genes. These results indicate that 17β-estradiol activates AMPK through an ER and activates Akt through AMPK activation in 3T3-L1 adipocytes, despite the absence of insulin. Furthermore, 17β-estradiol regulates the expression of genes related to glucose metabolism through ER-AMPK activation in these cells.
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October 2012
Volume 30 Issue 4

Print ISSN: 1107-3756
Online ISSN:1791-244X

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Spandidos Publications style
Kim J, Jo K, Kim B, Baik H and Lee S: 17β-estradiol induces an interaction between adenosine monophosphate-activated protein kinase and the insulin signaling pathway in 3T3-L1 adipocytes. Int J Mol Med 30: 979-985, 2012
APA
Kim, J., Jo, K., Kim, B., Baik, H., & Lee, S. (2012). 17β-estradiol induces an interaction between adenosine monophosphate-activated protein kinase and the insulin signaling pathway in 3T3-L1 adipocytes. International Journal of Molecular Medicine, 30, 979-985. https://doi.org/10.3892/ijmm.2012.1070
MLA
Kim, J., Jo, K., Kim, B., Baik, H., Lee, S."17β-estradiol induces an interaction between adenosine monophosphate-activated protein kinase and the insulin signaling pathway in 3T3-L1 adipocytes". International Journal of Molecular Medicine 30.4 (2012): 979-985.
Chicago
Kim, J., Jo, K., Kim, B., Baik, H., Lee, S."17β-estradiol induces an interaction between adenosine monophosphate-activated protein kinase and the insulin signaling pathway in 3T3-L1 adipocytes". International Journal of Molecular Medicine 30, no. 4 (2012): 979-985. https://doi.org/10.3892/ijmm.2012.1070