Hepatic miR-215 target Rictor and modulation of hepatic insulin signalling in rats

Increasing evidence has suggested that hepatic lipid accumulation is associated with hepatic insulin resistance; however, the underlying mechanism is yet to be determined. It was demonstrated that the levels of microRNA-215 (miR-215) expression in the liver of rats fed a high-fat diet were significantly increased compared with rats on a control diet. Additionally, it was revealed via luciferase assays and western blotting that miR-215 targets rapamycin-insensitive companion of mammalian target of rapamycin (Rictor), an important protein in the hepatic insulin signalling pathway. Following overexpression of miR-215 in the H4IIE rat hepatocarcinoma cell line, it was reported that the intracellular insulin signalling pathway was inhibited; conversely, inhibition of miR-215 expression induced this pathway. Furthermore, it was demonstrated via reverse transcription-quantitative polymerase chain reaction analysis that free fatty acids promoted the expression of miR-215. The present study provided a novel mechanistic insight into the association between nonalcoholic fatty liver and hepatic insulin resistance.