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. 2015 Oct 15;7(2):155–165. doi: 10.1111/jdi.12424

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© 2015 The Authors. Journal of Diabetes Investigation published by Asian Association of the Study of Diabetes (AASD) and Wiley Publishing Asia Pty Ltd

This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

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Pro‐inflammatory activation and amyloid deposition in the islet of type 2 diabetes. In the islet of type 2 diabetes, there is an increase in macrophage infiltration particular to pro‐inflammatory type 1. Amyloid deposition accelerates macrophage migration, and the release of cytokines and inflammasomes, such as Nlrp3 and interleukin‐1β (IL‐1β). IL‐1β in turn elicits β‐cell injury to disturb insulin secretion. Amyloid fibrils and oligomers are toxic to β‐cells, and augment the cell death pathway through oxidative stress, endoplasmic reticulum (ER) stress or autophagy deficits. IL‐1βR, interleukin‐1β receptor.