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. 2017 Oct 16;7:13248. doi: 10.1038/s41598-017-13251-0

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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STO-609 inhibition of the effect of NaHS to stimulate the insulin signalling pathway and AMPK to improve glucose uptake in the IR cell model. (a) C2C12 myoblasts were treated with the CaMKKβ inhibitor, STO-609 (25 μM, 30 min), and stimulated with or without insulin (10 nM, 10 min). STO-609 blocked the phosphorylation of IRS1, PI3K, AKT and AMPK induced by NaHS. (b) Additional increases of the NaHS-induced 2-NBDG uptake was blocked by STO-609 (25 μM, 30 min) in PA-induced IR C2C12 cells. **p < 0.01, ***p < 0.001. Data are shown as the mean ± sem.