Kim Mi-Kyung, Kim Hye-Soon, Lee In-Kyu, Park Keun-Gyu
Department of Internal Medicine, Keimyung University School of Medicine, Daegu 700-712, Republic of Korea.
Exp Diabetes Res. 2012;2012:509437. doi: 10.1155/2012/509437. Epub 2012 Mar 5.
Insulin resistance and pancreatic beta cell dysfunction are major contributors to the pathogenesis of diabetes. Various conditions play a role in the pathogenesis of pancreatic beta cell dysfunction and are correlated with endoplasmic reticulum (ER) stress. Pancreatic beta cells are susceptible to ER stress. Many studies have shown that increased ER stress induces pancreatic beta cell dysfunction and diabetes mellitus using genetic models of ER stress and by various stimuli. There are many reports indicating that ER stress plays an important role in the impairment of insulin biosynthesis, suggesting that reduction of ER stress could be a therapeutic target for diabetes. In this paper, we reviewed the relationship between ER stress and diabetes and how ER stress controls insulin biosynthesis.
胰岛素抵抗和胰腺β细胞功能障碍是糖尿病发病机制的主要促成因素。多种情况在胰腺β细胞功能障碍的发病机制中起作用,并与内质网(ER)应激相关。胰腺β细胞对内质网应激敏感。许多研究表明,使用内质网应激的遗传模型并通过各种刺激,内质网应激增加会诱导胰腺β细胞功能障碍和糖尿病。有许多报道表明内质网应激在胰岛素生物合成受损中起重要作用,这表明减轻内质网应激可能是糖尿病的一个治疗靶点。在本文中,我们综述了内质网应激与糖尿病之间的关系以及内质网应激如何控制胰岛素生物合成。