脂肪组织特异性Sirt6基因敲除小鼠发生非酒精性脂肪肝

Adipose tissu E-specific deletion of SIRT6 induces NAFLD

为了探讨脂肪组织特异性Sirt6基因敲除对小鼠肝脏的影响,利用CrE-LoxP系统获得脂肪组织特异性Sirt6基因敲除小鼠的基础上,通过组织病理学检查,Sirt6基因敲除小鼠和野生型小鼠的肝脏组织形态,进而提取两种基因型小鼠的肝脏组织RNA,通过实时定量PCR分析肝脏中参与脂肪生成的关键基因以及炎症标记物的表达水平。结果显示,成功获得脂肪组织特异性Sirt6基因敲除小鼠,组织病理学检查表明,无论是正常饮食还是高脂饮食,Sirt6基因敲除后小鼠均会发生脂肪肝并伴有炎症反应;此外,实时定量PCR的分析结果也显示,肝脏组织中参与脂肪生成的关键基因以及炎症标记物的表达均有明显升高。表明脂肪组织特异性Sirt6基因敲除小鼠发生非酒精性脂肪肝。

To study the effect of adipose tissuE-specific deletion of SIRT6 on the li~~er in mice. Methods： A mouse model of con- ditionally disrupting the Sift6 gene in fat using CrE-Loxp system was created. Histopathology examination was used to compare the hepatic tissue morphology of wild-type mice with that of S/rt6 gene knockout mice. Besides, real-time PCR was also employed to ex plore the expression levels of genes involved in lipogenesis and inflammation. Results： Sift6 mutant mice developed hepatosteatosis with macrophage infiltration both on chow diet and HFD. Consistently, real-time PCR revealed a significant increase in the expression levels of lipogenic and inflammatory genes. Conclusion：Adipose tissuE-specific gene Sirt6 ablation in mice leads to non-alcoholic fat- ty liver disease （NAFLD）.