Metabolic diseases including type 2 diabetes are associated with meta-inflammation. β-Cell failure is a major component of the pathogenesis of type 2 diabetes. It is now well established that increased numbers of innate immune cells, cytokines, and chemokines have detrimental effects on islets in these chronic conditions. Recently, evidence emerged which points to initially adaptive and restorative functions of inflammatory factors and immune cells in metabolism. In the following review, we provide an overview on the features of islet inflammation in diabetes and models of prediabetes. We separately emphasize what is known on islet inflammation in humans and focus on in vivo animal models and how they are used to elucidate mechanistic aspects of islet inflammation. Further, we discuss the recently emerging physiologic signaling role of cytokines during adaptation and normal function of islet cells.

中文翻译：

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2型糖尿病的胰岛炎症。

包括2型糖尿病在内的代谢性疾病与炎症相关。β细胞衰竭是2型糖尿病发病机理的主要组成部分。现已公认，在这些慢性病中，先天免疫细胞，细胞因子和趋化因子数量的增加对胰岛具有有害作用。最近，有证据表明炎症因子和免疫细胞在代谢中具有最初的适应性和恢复性功能。在下面的评论中，我们概述了糖尿病和前驱糖尿病模型中的胰岛炎症特征。我们分别强调人类胰岛炎症的已知知识，并着重于体内动物模型以及它们如何用于阐明胰岛炎症的机制方面。进一步，