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. 2017 Nov 20;24:87. doi: 10.1186/s12929-017-0394-0

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© The Author(s). 2017

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 3 — Potential role of ZIP7-mediated glucose metabolism in skeletal muscle. The ZIP7-gated release of zinc from the Golgi apparatus and/or the endoplasmic reticulum activates the phosphorylation of AKT and the subsequent mobilization of the glucose transporter GLUT4 which in turn brings glucose into the cytosol. Zinc also inactivates the negative regulation of insulin signalling, PTP-1B which allows the insulin signalling cascade process. The role of zinc activation of insulin receptor substrates (IRS) is not known (dashed lines)