Objective: Non-alcoholic fatty liver disease (NAFLD) has emergedas a common public health problem that can progress to end-stage liverdisease. Although the function of aquaglyceroporin-9(AQP9) as a glycerolchannel has been proven, the mechanism of AQP9in the development ofNAFLD is poorly understood. To investigate the effect of hepatic glyceroluptake inhibition, we utilized a lentivirus-associated RNA interferencetechnique to knock down the expression of hepatic AQP9in high fat diet(HFD) induced NAFLD in rodents.Methods: Male Sprague-Dawley rats were fed with standard chowdiet or HFD for8weeks, respectively. Rats fed with HFD were separatedinto3groups: HFD, control and transfection group, which were injectedwith equivalent PBS, lentivirus-scramble and lentivirus-shRNA-AQP9through hepatic portal vein, respectively.Results: The results demonstrated that transfection group revealed aremarkable decrease in expression of AQP9mRNA and protein in rat liver,furthermore, a milder degree of hepatic steatosis when compared to HFDand control groups at the end of8weeks. Conclusion: The down-regulation of AQP9expression alleviates highfat diet-induced NAFLD in rat liver tissue. Our results indicated a potentialrole for AQP9in pathogenesis of hepatic steatosis. |