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. 2018 Oct 25;9:630. doi: 10.3389/fendo.2018.00630

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Copyright © 2018 Guo, Xiao, Wang, Yao, Liao, Yu, Zhang, Zhang, Zheng, Ren and Gong.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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The potential mechanism of sodium butyrate on STZ-induced type 1 diabetes. STZ, specifically destroys pancreatic β-cells. The damaged β-cells passively release HMGB1 (11). At the same time, the islets are infiltrated by inflammatory cells such as DCs, macrophages and T cells. Naïve CD4⁺ T cells are differentiated into effector Th1 and/or Th17 cells based on their cytokine microenvironment. In addition, the released extracellular HMGB1 targets DCs or macrophage via the corresponding surface receptor(s), induces a signaling cascade and activates NF-κB pathway (12), therefore leading to the production of proinflammatory cytokines IL-1β, TNF-α, and IL-6 (49). the unbalanced Th1/Th2/Th17 and proinflammatory cytokines further accelerate the islets inflammation and β-cells destruction and lead to the onset of type 1 diabetes. Sodium butyrate, as a direct HMGB1 antagonist, could down-regulate the expression of HMGB1 and mediate the balance of Th1/Th2/Th17 paradigm, thus attenuating type 1 diabetes.