Type 2 diabetes mellitus:From a metabolic disorder to an inflammatory condition  

作　　者：Iqra Hameed Shariq R Masoodi Shahnaz A Mir Mudasar Nabi Khalid Ghazanfar Bashir A Ganai 

机构地区：[1]Department of Biochemistry,University of Kashmir [2]Department of Endocrin-ology,Sher-I-Kashmir Institute of medical Sciences [3]Division of Endocrinology,Diabetes and Nutrition,University of Maryland School of Medicine [4]Centre for Research and Development,Uni-versity of Kashmir

出　　处：《World Journal of Diabetes》2015年第4期598-612,共15页世界糖尿病杂志（英文版）（电子版）

基　　金：Supported by Department of Science and Technology,Government of India to Iqra Hameed,No.Wos-A LS 509/2012

摘　　要：Diabetes mellitus is increasing at an alarming rate and has become a global challenge.Insulin resistance intarget tissues and a relative deficiency of insulin secretion from pancreatic β-cells are the major features of type 2 diabetes(T2D).Chronic low-grade inflammation in T2 D has given an impetus to the field of immuno-metabolism linking inflammation to insulin resistance and β-cell dysfunction.Many factors advocate a causal link between metabolic stress and inflammation.Numerous cellular factors trigger inflammatory signalling cascades,and as a result T2 D is at the moment considered an inflammatory disorder triggered by disordered metabolism.Cellular mechanisms like activation of Tolllike receptors,Endoplasmic Reticulum stress,and inflammasome activation are related to the nutrient excess linking pathogenesis and progression of T2 D with inflammation.This paper aims to systematically review the metabolic profile and role of various inflammatory pathways in T2 D by capturing relevant evidence from various sources.The perspectives include suggestions for the development of therapies involving the shift from metabolic stress to homeostasis that would favour insulin sensitivity and survival of pancreatic β-cells in T2 D.Diabetes mellitus is increasing at an alarming rate andhas become a global challenge. Insulin resistance intarget tissues and a relative deficiency of insulin secretionfrom pancreatic β-cells are the major features of type 2diabetes （T2D）. Chronic low-grade inflammation in T2Dhas given an impetus to the field of immuno-metabolismlinking inflammation to insulin resistance and β-celldysfunction. Many factors advocate a causal link betweenmetabolic stress and inflammation. Numerouscellular factors trigger inflammatory signalling cascades,and as a result T2D is at the moment considered aninflammatory disorder triggered by disordered metabolism.Cellular mechanisms like activation of Tolllikereceptors, Endoplasmic Reticulum stress, andinflammasome activation are related to the nutrientexcess linking pathogenesis and progression of T2D withinflammation. This paper aims to systematically reviewthe metabolic profile and role of various inflammatorypathways in T2D by capturing relevant evidence fromvarious sources. The perspectives include suggestionsfor the development of therapies involving the shiftfrom metabolic stress to homeostasis that would favourinsulin sensitivity and survival of pancreatic β-cells inT2D.

关 键 词：Diabetes MELLITUS Inflammation INSULINRESISTANCE β-cell DYSFUNCTION ADIPOSE tissue 

分 类 号：R587.1[医药卫生—内分泌]