Background and study aims

To identify the roles and interaction of farnesoid X receptor (FXR) and peroxisome proliferator activated receptors (PPARs) in Non-alcoholic fatty liver disease (NAFLD) pathogenesis.

Material and Methods

16 C57/BL male FXR knockout (KO) mice and sex- and age-matched C57/BL wild type mice were received either standard rodent chow or high-fat and sucrose diet (Blank control, NAFLD, FXR KO and FXR KO NAFLD) for 8 weeks. After that, all mice were sacrificed. Liver tissues and blood samples were collected for laboratory and RT-PCR examination.

Results

NAFLD, FXR KO and FXR KO NAFLD mouse models were successful established. Compared with blank control, FXR and PPAR-α mRNA expression decreased significantly (P < 0.05), PPAR-β expression increased slightly (P > 0.05), PPAR-γ expression increased significantly in NAFLD (P < 0.05). Slight increased PPAR-α mRNA expression (P > 0.05) and markedly decreased PPAR-β and PPAR-γ expression (P < 0.05) were found in FXR KO. Compared with FXR KO group, there was a slight increase in PPAR-αand PPAR-βmRNA expression (P > 0.05) and significant increase in PPAR-γ expression (P < 0.05) in FXR KO NAFLD group. Comparison with NAFLD, PPAR-α mRNA expression increased slightly (P > 0.05), PPAR-β and PPAR-γ expression decreased significantly (P < 0.05) in FXR KO NAFLD.

Conclusion

FXR and PPARs interaction may play important roles in NAFLD pathogenesis.

中文翻译：

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FXR 和 PPARs 在非酒精性脂肪肝发病机制中的作用和相互作用。

背景和研究目的

确定法尼醇X 受体 ( FXR ) 和过氧化物酶体增殖物激活受体 ( PPAR ) 在非酒精性脂肪肝 (NAFLD) 发病机制中的作用和相互作用。

材料与方法

16 只 C57/BL 雄性FXR敲除 (KO) 小鼠和性别和年龄匹配的 C57/BL 野生型小鼠接受标准啮齿动物食物或高脂肪和蔗糖饮食（空白对照、NAFLD、FXR KO 和FXR KO NAFLD） 8 周。之后，处死所有小鼠。收集肝组织和血液样本用于实验室和 RT-PCR 检查。

结果

成功建立NAFLD、FXR KO和FXR KO NAFLD小鼠模型。与空白对照相比，NAFLD中FXR和PPAR-α mRNA表达显着降低（P  < 0.05），PPAR-β表达略有增加（P  > 0.05），PPAR-γ表达显着增加（P  < 0.05）。 在FXR KO中发现PPAR-α mRNA 表达略有增加（P  > 0.05），PPAR-β和PPAR-γ表达显着降低（P < 0.05）。与FXR相比KO组中，FXR KO NAFLD组PPAR-α和PPAR-β mRNA表达略有增加（P  > 0.05），PPAR-γ表达显着增加（P  < 0.05）。与NAFLD相比，FXR KO NAFLD中PPAR-α mRNA表达略有增加（P  > 0.05），PPAR-β和PPAR-γ表达显着降低（P  < 0.05）。

结论

FXR和PPARs相互作用可能在 NAFLD 发病机制中发挥重要作用。