Ehses Jan A, Ellingsgaard Helga, Böni-Schnetzler Marianne, Donath Marc Y
Division of Endocrinology, Diabetes and Nutrition, Center for Integrated Human Physiology, University Hospital of Zürich, 8091 Zürich, Switzerland.
Arch Physiol Biochem. 2009 Oct;115(4):240-7. doi: 10.1080/13813450903025879.
Evidence in support of the concept of local pancreatic islet inflammation as a mechanism of beta cell failure in type 2 diabetes is accumulating. Observations in human islets from type 2 diabetic patients and rodent models of the disease indicate the increased presence of IL-1 driven cytokines and chemokines in pancreatic islets, concomitant with immune cell infiltration. Inflammation is the body's protective response to harmful stimuli and tissue damage. However, under chronic stress (e.g. metabolic stress in obesity and type 2 diabetes) the body's own defensive response may become deleterious to tissue function. Here, we summarize the current evidence that islet inflammation is a feature of type 2 diabetes, and discuss its role with respect to alpha and beta cell compensation and eventual beta cell failure.
支持局部胰岛炎症是2型糖尿病β细胞功能衰竭机制这一概念的证据正在不断积累。对2型糖尿病患者的人类胰岛以及该疾病啮齿动物模型的观察表明，胰岛中白细胞介素-1驱动的细胞因子和趋化因子增多，同时伴有免疫细胞浸润。炎症是机体对有害刺激和组织损伤的保护性反应。然而，在慢性应激（如肥胖和2型糖尿病中的代谢应激）下，机体自身的防御反应可能会对组织功能产生有害影响。在此，我们总结了目前关于胰岛炎症是2型糖尿病特征的证据，并讨论了其在α细胞和β细胞代偿以及最终β细胞功能衰竭方面的作用。
