摘要
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、AMPK_(α1)、ACC、P-AMPK_(αT183/T172)、P-ACC_(S79)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-AMPK_(αT183/T172)/AMPK_(α1)、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,AMPK_(α1),ACC,P-AMPK_(αT183/T172) and P-ACC_(S79) protein.Results:Zicui Jiangtang prescription 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-AMPK_(αT183/T172) and P-ACC_(S79)/ACC protein.Conclusion:Zicui Jiangtang prescription could alleviate IR of liver in obese mice possibly via Fetuin B-AMPK/ACC signaling pathway.
作者
刘曼曼
冯珍凤
胡春平
陈见纺
沈怡华
高俊凤
严军
LIU Manman;FENG Zhenfeng;HU Chunping;CHEN Jianfang;SHEN Yihua;GAO Junfeng;YAN Jun(Shanghai City Jiading District Hospital of Traditional Chinese Medicine,Shanghai 201899,China;Graduate School,Shanghai University of Traditional Chinese Medicine,Shanghai 201203,China)
出处
《西部中医药》
2024年第2期14-19,共6页
Western Journal of Traditional Chinese Medicine
基金
上海市嘉定区科委项目(JDKW-2019-W17)
上海市“十四五”中医特色专科项目(ZYTSZK1-10)
上海市嘉定区卫健委项目(2023-KY-ZYY-03)。
