Insulin　resistance　(IR)　is　a　complex　pathological　condition　resulting　from　the　dysregulation　of　cellular　response　to　insulin　hormone　in　insulin-dependent　cells　and　is　recognized　as　a　pathogenic　hallmark　and　strong　risk　factor　for　metabolic　syndrome.　The　present　study　aims　to　elucidate　the　molecular　mechanism　of　the　pathogenesis　of　IR.　Here,　we　used　human　umbilical　vein　endothelial　cells　(HUVECs)　to　establish　the　IR　cell　model　induced　by　1　x　10(-6)　mmol/L　insulin.　After　48　h,　reactive　oxygen　species　(ROS)　and　glucose　consumption　were　measured　by　DCFH-DA　and　GOD-POD　methods,　respectively.　The　results　of　Microarray　analysis　demonstrated　that　there　were　10　differentially　expressed　miRNAs　(DEMs)　selected　based　on　Fold　change　(FC)　and　P　value　in　the　IR　cell　model　compared　with　HUVECs.　The　enriched　gene　ontology　(GO)　terms　analysis　showed　that　the　target　genes　of　these　10　DEMs　were　significantly　enriched　in　biological　process,　cellular　component　and　molecular　function,　and　the　significantly　enriched　Kyoto　Encyclopedia　of　Genes　or　Genomes　(KEGG)　pathways　mainly　include　AMPK　signaling　pathway　and　PI3K　signaling　pathway.　Amongst　all,　the　expression　level　of　miR-3138　was　highest　in　the　IR　cell　model　evaluated　by　qRT-PCR.　Through　Targetscan,　KSR2　mRNA　was　predicted　as　a　target　of　miR-3138.　And　mRNA　and　protein　expression　levels　of　miR-3138,　KSR2,　GLUT4,　AMPK,　PI3K,　Akt　were　examined　using　qRT-PCR　and　Western　blotting,　respectively.　The　interaction　between　miR-3138　and　KSR2　was　evaluated　by　dual-luciferase　reporter　assay.　Our　results　showed　that　miR-3138　significantly　deteriorated　the　IR　of　HUVECs　via　KSR2/AMPK/GLUT4　signaling　pathway.