CAJ | 학술논문

慢性高糖可损伤胰岛β细胞,这被称为“葡萄糖毒性”.胰岛β细胞葡萄糖毒性涉及多种机制包括氧化应激、内质网应激、线粒体功能失调、炎症、糖基化终末产物形成、低氧状态与低氧诱导因子激活、胰岛β细胞分化表型丧失,等等.目前认为,氧化应激、内质网应激和胰岛β细胞分化表型的丧失在胰岛β细胞葡萄糖毒性中的作用较为明确;其中氧化应激在糖尿病胰岛β细胞葡萄糖毒性中发挥中心性作用.
만성고당가손상이도β세포,저피칭위“포도당독성”.이도β세포포도당독성섭급다충궤제포괄양화응격、내질망응격、선립체공능실조、염증、당기화종말산물형성、저양상태여저양유도인자격활、이도β세포분화표형상실,등등.목전인위,양화응격、내질망응격화이도β세포분화표형적상실재이도β세포포도당독성중적작용교위명학;기중양화응격재당뇨병이도β세포포도당독성중발휘중심성작용.
The deterioration of beta-cell function and survival caused by chronic high glucose exposure is termed glucotoxicity.The mechanisms of pancreatic beta-cell glucotoxicity involve in oxidative stress,endoplasmic reticulum stress,mitochrondrial dysfunction,inflammation,advanced glycation end products,hypoxia and activation of HIF-1 α,and loss of differentiation in the alteration of beta-cell phenotype.The role of oxidative stress,endoplasmic reticulum stress,and loss of differentiation in the alteration of beta-cell phenotype is well ascertained.Oxidative stress is the central mechanism for glucotoxicity in pancreatic beta cells in diabetes.