CAJ | 학술논문

“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-inflammatory cytokine),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.
“이도염”시1형당뇨병환자중요적조직병이학개변.연이,재2형당뇨병환자,이도야출현거서세포침윤화산생촉염성세포인자(pro-inflammatory cytokine),제시2형당뇨병환자야존재“이도염”,저시가도치이도β세포공능결함적원인.만성고당、유리지방산(FFA)、수소화인이도정분양다태(hIAPP)도가유도이도촉염성세포인자적산생;촉염성세포인자래원우이도β세포화/혹거서세포.촉염성세포인자가통과내질망응격、양화응격화선립체공능실조인기이도β세포공능결함화세포조망.항염치료가개선2형당뇨병환자화2형당뇨병동물모형이도β세포공능화혈당공제.
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 (hIAPP) 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 function and blood glucose control in the patients and the rodent models of type 2 diabetes.