促炎性细胞因子在2型糖尿病胰岛β细胞功能缺陷中的作用

Role of pro-inflammatory cytokine in dysfunction of pancreatic beta-cell in patients with type 2 diabetes

“胰岛炎”是1型糖尿病患者重要的组织病理学改变。然而，在2型糖尿病患者，胰岛也出现巨噬细胞浸润和产生促炎性细胞因子（pro—inflammatorycytokine），提示2型糖尿病患者也存在“胰岛炎”，这是可导致胰岛β细胞功能缺陷的原因。慢性高糖、游离脂肪酸（FFA）、瘦素和人胰岛淀粉样多肽（hIAPP）都可诱导胰岛促炎性细胞因子的产生；促炎性细胞因子来源于胰岛β细胞和／或巨噬细胞。促炎性细胞因子可通过内质网应激、氧化应激和线粒体功能失调引起胰岛β细胞功能缺陷和细胞凋亡。抗炎治疗可改善2型糖尿病患者和2型糖尿病动物模型胰岛β细胞功能和血糖控制。

Insulitis is the prominent histopathological feature of type 1 diabetes. However, islets from patients with type 2 diabetes displays the presence of pro-inflammatory cytokines and macrophage infiltration, indicating that insulitis also occurs in type 2 diabetes, which might contribute to pancreatic beta-cell dysfunction. Exposed to chronic high glucose, free fatty acid （FFA）, leptin, or human islet amyloid polypeptide （hlAPP） induce the production of pro-inflammatory cytokines, which originates from pancreatic beta cells and （or） infiltrating macrophages. Pro-inflammatory cytokines might cause pancreatic beta-cell dysfunction and apoptosis via endoplasmic reticulum stress, oxidative stress, and mitochondrial dysfunction. Anti-inflammatory treatment improves pancreatic beta-cell fimction and blood glucose control in the patients and the rodent models of type 2 diabetes.