Chronic, unresolved tissue inflammation is a well-described feature of obesity, type 2 diabetes mellitus (T2DM) and other insulin-resistant states. In this context, adipose tissue and liver inflammation have been particularly well studied; however, abundant evidence demonstrates that inflammatory processes are also activated in pancreatic islets from obese animals and humans with obesity and/or T2DM. In this Review, we focus on the characteristics of immune cell-mediated inflammation in islets and the consequences of this with respect to β-cell function. In contrast to type 1 diabetes mellitus, the dominant immune cell type causing inflammation in obese and T2DM islets is the macrophage. The increased macrophage accumulation in T2DM islets primarily arises through local proliferation of resident macrophages, which then provide signals (such as platelet-derived growth factor) that drive β-cell hyperplasia (a classic feature of obesity). In addition, islet macrophages also impair the insulin secretory capacity of β-cells. Through these mechanisms, islet-resident macrophages underlie the inflammatory response in obesity and mechanistically participate in the β-cell hyperplasia and dysfunction that characterizes this insulin-resistant state. These findings point to the possibility of therapeutics that target islet inflammation to elicit beneficial effects on β-cell function and glycaemia.

中文翻译：

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巨噬细胞在肥胖相关胰岛炎症和 β 细胞异常中的作用。

慢性、未解决的组织炎症是肥胖、2 型糖尿病 (T2DM) 和其他胰岛素抵抗状态的一个充分描述的特征。在这种情况下，脂肪组织和肝脏炎症得到了特别好的研究。然而，大量证据表明，肥胖动物和患有肥胖症和/或 T2DM 的人的胰岛也会激活炎症过程。在这篇综述中，我们关注胰岛中免疫细胞介导的炎症的特征及其对 β 细胞功能的影响。与 1 型糖尿病相比，在肥胖和 T2DM 胰岛中引起炎症的主要免疫细胞类型是巨噬细胞。T2DM 胰岛中巨噬细胞积累的增加主要是通过常驻巨噬细胞的局部增殖产生的，然后提供驱动 β 细胞增生（肥胖的典型特征）的信号（例如血小板衍生的生长因子）。此外，胰岛巨噬细胞也会损害 β 细胞的胰岛素分泌能力。通过这些机制，胰岛驻留巨噬细胞是肥胖症炎症反应的基础，并且机械地参与了表征这种胰岛素抵抗状态的 β 细胞增生和功能障碍。这些发现指出了针对胰岛炎症的治疗方法对 β 细胞功能和血糖产生有益影响的可能性。胰岛常驻巨噬细胞是肥胖症炎症反应的基础，并在机制上参与了表征这种胰岛素抵抗状态的 β 细胞增生和功能障碍。这些发现指出了针对胰岛炎症的治疗方法对 β 细胞功能和血糖产生有益影响的可能性。胰岛常驻巨噬细胞是肥胖症炎症反应的基础，并在机制上参与了表征这种胰岛素抵抗状态的 β 细胞增生和功能障碍。这些发现指出了针对胰岛炎症的治疗方法对 β 细胞功能和血糖产生有益影响的可能性。