Insulitis in type 2 diabetes
Insulitis in type 2 diabetes
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DOI：
10.1111/j.1463-1326.2008.00950.x
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发表时间：
2008-11-01
影响因子：
5.8
通讯作者：
Donath, M. Y.
中科院分区：
文献类型：
--
作者：
Boeni-Schnetzler, M.;Ehses, J. A.;Donath, M. Y.
2型糖尿病患者的胰岛具有细胞因子存在所反映的特征或炎症过程。免疫细胞、β细胞凋亡、淀粉样蛋白沉积和纤维化。事实上，β-细胞从病人的类型。2型糖尿病显示炎症标志物，包括白细胞介素（IL）-1 β表达增加。此外，在人类2型糖尿病患者和大多数糖尿病动物模型中观察到胰岛相关巨噬细胞增加。重要的是，在糖尿病发作之前，在高脂肪喂养的小鼠胰岛中可以很早检测到巨噬细胞数量的增加。这些免疫细胞最有可能被胰岛衍生的趋化因子所吸引，这些趋化因子是在代谢应激反应中产生的。并在IL-1 β的控制下。因此，调节胰岛内炎症介质，特别是IL-1 β，可以预防2型糖尿病中的胰岛炎，因此将其本身作为一种可能的具有疾病改善潜力的Casal疗法。
Islets of patients with type 2 diabetes have the feature or an inflammatory process reflected by the presence of cytokines. immune cells, beta-cell apoptosis, amyloid deposits and fibrosis. Indeed, beta-cells from patients with type. 2 diabetes display inflammatory markers, including increased interleukin (IL)-1 beta expression. Furthermore, increased islet-associated macrophages are observed in human type 2 diabetic patients and in most animal models of diabetes. Importantly increased numbers of macrophages are detectable very early in high fat-fed mice islets, before the onset of diabetes. These immune cells are most likely attracted by islet-derived chemokines, produced in response to metabolic: stress. and under the control of IL-1 beta. It follows that modulation of intra-islet inflammatory, mediators, in particular IL-1 beta may prevent insulitis in type 2 diabetes and therefore presents itself as a possible casal therapy with disease-modifying potential.