Role of inflammatory mechanisms in pathogenesis of type 2 diabetes mellitus

被引:322
|
作者
Akash, Muhammad Sajid Hamid [1 ,2 ]
Rehman, Kanwal [1 ]
Chen, Shuqing [1 ]
机构
[1] Zhejiang Univ, Coll Pharmaceut Sci, Inst Pharmacol Toxicol & Biochem Pharmaceut, Hangzhou 310058, Zhejiang, Peoples R China
[2] Univ Faisalabad, Govt Coll, Coll Pharm, Faisalabad, Pakistan
关键词
PRO-INFLAMMATORY CYTOKINES; OXIDATIVE STRESS; HYPERGLYCEMIA; DYSLIPIDEMIA; INTERLEUKIN-1 RECEPTOR ANTAGONIST; BETA-CELL DYSFUNCTION; INTERLEUKIN-1 RECEPTOR ANTAGONIST; ENDOPLASMIC-RETICULUM STRESS; ACTIVATED SIGNALING PATHWAYS; INDUCED INSULIN-RESISTANCE; ADIPOSE-TISSUE; OXIDATIVE STRESS; ISLET INFLAMMATION; PANCREATIC-ISLETS; HIGH GLUCOSE;
D O I
10.1002/jcb.24402
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Type 2 diabetes mellitus (T2DM) is characterized by progressive beta-cell dysfunctioning and insulin resistance. This article reviews recent literature with special focus on inflammatory mechanisms that provoke the pathogenesis of T2DM. We have focused on the recent advances in progression of T2DM including various inflammatory mechanisms that might induce inflammation, insulin resistance, decrease insulin secretion from pancreatic islets and dysfunctioning of beta-cells. Here we have also summarized the role of various pro-inflammatory mediators involved in inflammatory mechanisms, which may further alter the normal structure of beta-cells by inducing pancreatic islet's apoptosis. In conclusion, it is suggested that the role of inflammation in pathogenesis of T2DM is crucial and cannot be neglected. Moreover, the insight of inflammatory responses in T2DM may provide a new gateway for the better treatment of diabetes mellitus. J. Cell. Biochem. 114: 525531, 2013. (C) 2012 Wiley Periodicals, Inc.
引用
收藏
页码:525 / 531
页数:7
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