title: Reduction of insulin resistance in HepG2 cells by knockdown of LITAF expression in human THP-1 macrophages.
abstract: 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 expression 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 polymerase 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.
authors.affiliation: Department of Endocrinology, Zhongnan Hospital of Wuhan University, Wuhan, 430071, China.
authors.forename: Yan
authors.initials: Y
authors.lastname: Huang
authors.affiliation: Department of Endocrinology, Zhongnan Hospital of Wuhan University, Wuhan, 430071, China.
authors.forename: Jie
authors.initials: J
authors.lastname: Liu
authors.affiliation: Department of Endocrinology, Zhongnan Hospital of Wuhan University, Wuhan, 430071, China. oxyc2007@yahoo.com.cn.
authors.forename: Yancheng
authors.initials: Y
authors.lastname: Xu
authors.affiliation: Department of Endocrinology, Zhongnan Hospital of Wuhan University, Wuhan, 430071, China.
authors.forename: Zhe
authors.initials: Z
authors.lastname: Dai
authors.affiliation: Department of Endocrinology, Zhongnan Hospital of Wuhan University, Wuhan, 430071, China.
authors.forename: Martins Hedson
authors.initials: MH
authors.lastname: Alves
mesh_terms: D002450:Cell Communication / Q000502:physiology*; D002454:Cell Differentiation / Q000502:physiology; D002460:Cell Line; D018920:Coculture Techniques; D055785:Gene Knockdown Techniques; D056945:Hep G2 Cells; D006801:Humans; D007333:Insulin Resistance / Q000502:physiology*; D008264:Macrophages / Q000166:cytology* / Q000502:physiology*; D009687:Nuclear Proteins / Q000378:metabolism*; D014157:Transcription Factors / Q000378:metabolism*
chemical_list: C118738:LITAF protein, human; D009687:Nuclear Proteins; D014157:Transcription Factors