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. 2019 Sep 6;9:12827. doi: 10.1038/s41598-019-49289-5

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© The Author(s) 2019

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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The proposed model. The elevated levels of proinflammatory cytokines, fatty acids and glucose play a key role in triggering beta cell stress and demise. Phlda3 is a novel adaptive beta cell stress response gene induced downstream of XBP1 that promotes beta cell survival via the repression of the NFκB pathway and the maintenance of adequate antioxidant and adaptive UPR gene expression. FFA; free fatty acids, NO; nitric oxide, ROS; reactive oxygen species, T1D; type 1 diabetes, T2D; type 2 diabetes.