目的:探讨滋膵降糖方通过Fetuin B-AMPK/ACC通路改善肥胖C57BL/6J小鼠胰岛素抵抗的机制.方法:高脂饮食喂养C57BL/6J小鼠,构建胰岛素抵抗模型,随机分为模型组、滋膵降糖方组、二甲双胍组、联合组(滋膵降糖方+二甲双胍),正常饮食小鼠为空白对照组.观察各组小鼠体质量、肝脏质量、葡萄糖耐量、胰岛素抵抗指数,肝脏Fetuin B、AMPK、ACC mRNA及肝脏Fetuin B、AMPKα1、ACC、P-AMPKαT183/T172、P-ACCS79蛋白表达.结果:滋膵降糖方可改善小鼠葡萄糖耐量,减小曲线下面积,降低胰岛素抵抗指数,下调肝脏质量和肝体比,降低肝脏Fetuin B、ACC mRNA和Fetuin B蛋白表达,上调AMPK mRNA和P-AMPKαT183/T172/AMPKα1、P-ACCs79/ACC蛋白水平.结论:滋膵降糖方可能通过Fetuin B-AMPK/ACC信号通路减轻肥胖小鼠肝脏胰岛素抵抗.
Objective:To explore the mechanism of improving insulin resistance in obese C57BL/6J mice via Fetuin B-AMPK/ACC pathway medicated by Zicui Jiangtang prescription.Methods:The models with insulin resistance(IR)were established by feeding C57BL/6J mice high-fat diet,and they were randomly allocated to the model group,Zicui Jiangtang prescription group,metformin group,the combination group(Zicui Jiangtang prescription+metformin),the mice fed normal diet were chosen as blank control group.To observe the mice's body mass,liver mass,glucose tolerance,insulin resistance index(IRI),the expressions of liver Fetuin B,AMPK,ACC mRNA,liver Fetuin B,AMPKα1,ACC,P-AMPKαT183/T172 and P-ACCS79 protein.Results:Zicui Jiangtang prescrip-tion could improve the mice'glucose tolerance,reduce area under the curve,lower IRI,liver mass and hepatocrit,cut down the expressions of liver Fetuin B,ACC mRNA and Fetuin B protein,up regulate the levels of AMPK mRNA,P-AMPKαT183/T172 and P-ACCS79/ACC protein.Conclusion:Zicui Jiangtang prescription could alleviate IR of liver in obese mice possibly via Fetuin B-AMPK/ACC signaling pathway.