Reduction of Insulin Resistance in HepG2 Cells by Knockdown of LITAF Expression in Human THP-1 Macrophages  

作　　者：黄艳 刘洁 徐焱成 代喆 

机构地区：[1]Martins Hedson Alves Department of Endocrinology,Zhongnan Hospital of Wuhan University

出　　处：《Journal of Huazhong University of Science and Technology(Medical Sciences)》2012年第1期53-58,共6页华中科技大学学报（医学英德文版）

基　　金：supported by grants from the National Natural Science Foundation of China (No. 30871188);the Natural Science Foundation of Hubei Province of China (No.3031314)

摘　　要：The molecular mechanism by which obesity induces insulin resistance is not completely understood.The aim of this study was to determine how lipopolysaccharide-induced tumor necrosis-α factor (LITAF) influenced obesity-induced insulin resistance using a cellular co-culture system.The cells were divided into 3 groups:palmitic acid (PA) stimulation group,LITAF small interfering RNA (siRNA) group and untreated (NC) group.The LITAF siRNA was used for knockdown of LITAF ex-pression in human THP-1 macrophages.The expression levels of LITAF,IRS-2,IRS-2Tyr465,PI3K,and GLUT2 in each group were measured by using quantitative reverse transcriptase real-time poly-merase chain reaction and Western blotting.The expression of LITAF was much higher in the PA group than in the siRNA and NC groups (P<0.05);meanwhile,the expression of IRS-2,IRS-2Tyr465,PI3K,and GLUT2 was much lower in the PA group than in the NC group (P<0.05);however,IRS-2,IRS-2Tyr465,PI3K,and GLUT2 had much higher expression in the siRNA group than in the PA group (P<0.05).It is concluded that PA can induce insulin resistance in liver cells and knockdown of LITAF expression can reduce insulin resistance in liver cells,suggesting LITAF may regulate the insulin signal transduction pathway involved in obesity-induced insulin resistance.The molecular mechanism by which obesity induces insulin resistance is not completely understood.The aim of this study was to determine how lipopolysaccharide-induced tumor necrosis-α factor (LITAF) influenced obesity-induced insulin resistance using a cellular co-culture system.The cells were divided into 3 groups:palmitic acid (PA) stimulation group,LITAF small interfering RNA (siRNA) group and untreated (NC) group.The LITAF siRNA was used for knockdown of LITAF ex-pression in human THP-1 macrophages.The expression levels of LITAF,IRS-2,IRS-2Tyr465,PI3K,and GLUT2 in each group were measured by using quantitative reverse transcriptase real-time poly-merase chain reaction and Western blotting.The expression of LITAF was much higher in the PA group than in the siRNA and NC groups (P<0.05);meanwhile,the expression of IRS-2,IRS-2Tyr465,PI3K,and GLUT2 was much lower in the PA group than in the NC group (P<0.05);however,IRS-2,IRS-2Tyr465,PI3K,and GLUT2 had much higher expression in the siRNA group than in the PA group (P<0.05).It is concluded that PA can induce insulin resistance in liver cells and knockdown of LITAF expression can reduce insulin resistance in liver cells,suggesting LITAF may regulate the insulin signal transduction pathway involved in obesity-induced insulin resistance.

关 键 词：DIABETES OBESITY insulin resistance INFLAMMATION lipopolysaccharide-induced tumor ne-crosis-α factor 

分 类 号：R587[医药卫生—内分泌]