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MicroRNA‐26a–interleukin (IL)‐6–IL‐17 axis regulates the development of non‐alcoholic fatty liver disease in a murine model

Non‐alcoholic fatty liver disease (NAFLD) is a hepatic presentation of obesity and metabolic syndrome. MicroRNA 26a (Mir‐26a) has been reported to play functions in cellular differentiation, cell growth, cell apoptosis and metastasis. A recent paper indicated that Mir‐26a regulated insulin sensitivity and metabolism of glucose and lipids. However, the role of Mir‐26a in NAFLD still needs to be investigated further. In our current study, vectors encoding pre‐Mir‐26a (LV‐26a) and an empty lentiviral vector (LV‐Con) delivered approximately 2 × 107 transforming units of recombinant lentivirus were injected into mice through the tail vein. LV‐26a‐infected mice were protected from glucose dysmetabolism and showed markedly decreased total liver weight, hepatic triglyceride deposition and serum alanine transaminase (ALT) concentration when compared with LV‐Con‐treated mice. LV‐26a‐treated mice also exhibited decreased infiltration of immune cells in the liver – something attributed to reduce infiltration of T cell receptor (TCR)‐γδ+, granulocyte‐differentiation antigen‐1 (Gr‐1)+ cells and CD11b+ cells. Next, we found that Mir‐26a inhibited the expression of interleukin (IL)−17 and IL‐6 in vivo and in vitro. Furthermore, the decreased expression of IL‐17 in the liver tissue induced by Mir‐26a was abrogated completely by IL‐6 overexpression. The decreased total liver weight, hepatic triglyceride deposition and serum ALT concentration induced by Mir‐26a was also abrogated completely by IL‐6 over‐expression. In conclusion, the Mir‐26a–IL‐6–IL‐17 axis regulates the development of NAFLD in a murine model.