[No authors listed]
The expression of microRNAâ802 (miRâ802) is known to be associated with insulin resistance (IR); however, the mechanism remains unclear. The present study investigated how miRâ802 contributes to the development of IR using C57BL/6J mice fed a highâfat diet (HFD) to establish a model of IR. Adenoâassociated virus overexpressing miRâ802 was administered to the mice via tail vein injection. The effects of miRâ802 on reactive oxygen species lipid peroxidation (LPO) and the activities of multiple enzymes were investigated. Western blot analysis was used to estimate the protein levels of extracellular signal regulated kinase (ERK), p38mitogenâactivated protein kinases (p38MAPK), câJun Nâterminal kinase (JNK), insulin receptor substrate 1 (IRSâ1) and protein kinase B (AKT1). The results demonstrated that the levels of and LPO production were increased in the livers of the miRâ802âtreated group compared with the control group. The activities of the duanyu1670ârelated enzymes were reduced. Furthermore, the expression of phosphorylated (phosphor)âp38MAPK and phosphorâJNK were upregulated in the miRâ802 overexpression group, whereas there was no difference in the expression levels of phosphorâERK. The expression levels of phosphorâAKT1 were reduced in the miRâ802âtreated group and these effects were reversed by miRâ802 knockdown. In conclusion, the results demonstrate that miRâ802 may cause IR by activating the JNK and p38MAPK pathways to increase hepatic oxidative stress.
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