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

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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… Click to show full abstract

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.

Keywords: insulin signalling; insulin; hepatic insulin; target; mir 215

Journal Title: Molecular Medicine Reports
Year Published: 2019

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