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AIM:To assess the regulatory effect of micro RNA-185(mi R-185)on lipid metabolism and the insulin signalling pathway in human Hep G2 hepatocytes and a high-fat diet mouse model.METHODS:Quantitative reverse transcription-polymerase chain reaction was used to assess the m RNA levels of lipogenic genes after loss or gain of mi R-185.In addition,the amounts of insulin signalling intermediates were determined after transfection of Hep G2 cells with pre-mi R-185.RESULTS:Mi R-185 levels decreased in a time-and dose-dependent manner in response to palmitic acid in human Hep G2 hepatocytes.Transfection of Hep G2 cells with mi R-185 significantly decreased the m RNA levels of fatty acid synthase,3-hydroxy-3-methylglutaryl-Co A reductase,sterol-regulatory element binding protein-2,and sterol-regulatory element binding protein-1c,whereas inhibition of mi R-185 using an anti-mi R-185oligonucleotide produced the opposite effect in Hep G2cells.In a high-fat diet mouse model,the accumulation of lipids was significantly improved after treatment with mi R-185,compared with control animals.Induction of mi R-185 enhanced the insulin signalling pathway by upregulating the insulin-receptor substrate-2.CONCLUSION:These findings suggest that mi R-185plays an important role in regulating fatty-acid metabolism and cholesterol homeostasis in hepatocytes,as well as in improving insulin sensitivity,both in vitro and in vivo.
AIM: To assess the regulatory effect of microRNA-185 (mi R-185) on lipid metabolism and the insulin signaling pathway in human Hep G2 hepatocytes and a high-fat diet mouse model. METHODS: Quantitative reverse transcription-polymerase chain reaction was used to assess the m RNA levels of lipogenic genes after loss or gain of mi R-185. addition, the amounts of insulin signaling intermediates were determined after transfection of Hep G2 cells with pre-mi R-185 .RESULTS: Mi R- 185 levels decreased in a time-and dose-dependent manner in response to palmitic acid in human Hep G2 hepatocytes. Transfection of Hep G2 cells with mi R-185 significantly decreased the m RNA levels of fatty acid synthase, 3-hydroxy-3- methylglutaryl-Co A reductase, sterol-regulatory element binding protein-2, and sterol-regulatory element binding protein-1c, thereafter inhibition of mi R-185 using an anti-mi R-185 oligonucleotide produced the opposite effect in Hep G2 cells. a high-fat diet mouse model, the accumulation of lipids was significantly improved after treatment with mi R-185, compared with control animals. Induction of mi R-185 enhanced the insulin signaling pathway by upregulating the insulin-receptor substrate-2.CONCLUSION: These findings suggest that mi R-185plays an important role in regulating fatty-acid metabolism and cholesterol homeostasis in hepatocytes, as well as in improving insulin sensitivity, both in vitro and in vivo.