黄芪多糖对饮食诱导小鼠肝脏胰岛素抵抗的预防作用  

Protective effect on hepatic insulin resistance of Astragalus polysaccharide in the high fat-fed mice model

作　　者：毛先晴[1] 欧阳静萍[1] 

机构地区：[1]武汉大学基础医学院病理生理学教研室,湖北武汉430079

出　　处：《中国病理生理杂志》2007年第11期2222-2225,共4页Chinese Journal of Pathophysiology

基　　金：国家自然科学基金资助项目(No30370673)

摘　　要：目的:探讨黄芪多糖(APS)对饮食诱导小鼠肝脏胰岛素抵抗的预防作用及其机制。方法:26只C57BL/6J小鼠随机分成正常对照(C)组(n=10)、胰岛素抵抗(IR)组和黄芪多糖预处理(IA)组(n=8)(溶液灌胃,700mg·kg-1.d-1,12周)。检测动物血糖、血胰岛素、肝脏TG、FFA;计算胰岛素敏感性;光镜及电镜下观察肝脏病理改变;免疫印记法检测肝脏GSK3β表达的改变。结果:12周后成功建立出胰岛素抵抗小鼠模型;APS可预防IR小鼠肝脂肪变性的发生;IA组体重、血糖、肝重、肝组织内TG、FFA含量均明显低于IR组(P<0.05);IA组GSK3β减低而ser9GSK3β高于IR组(P<0.01)。结论:APS治疗可明显改善高脂饮食诱导的胰岛素抵抗及肝脏脂肪变性,其机制与减少GSK3β表达及增加胰岛素刺激后SER9-GSK3β水平有关。AIM： To investigate the effect and mechanism of Astragalus polysaccharide （APS） on the amelio-ration of hepatic insulin resistance in high fat-fed mouse model METHODS： C57BL/6J mice （n = 26） were divided into three groups randomly： C group （ an animal model for control, n = 10） ; IR group （ an animal model of insulin resistance, n =8） and IA group （an animal model in high -fat diet with APS treatment forl2 weeks, 700mg·kg^-1·d^-1, ig）. High - fat diet was used to induce the formation of insulin resistant. The parameters and insulin sensitivity of the animals were observed. The pathological features of the liver were presented through microscope and TEM. The expression changes of hepatic GSK3β were measured by Western blotting RESULTS： In this study, the fat -fed mouse model of insulin resistance was established successfully. The mice in IA group responded to the 12 - week APS therapy with a significant decrease in the level of blood glucose, plasma insulin, body weight, hepatic TG/FFA and improved glucose tolerance compared with those in IR group. In addition, the expression and the activity of GSK3β were lower in IA group （ vs IR group, P 〈 0. 05）.We also found the hepatic steatosis could be significantly alleviated with APS therapy. CONCLUSION： These results indicate that APS prevents the occurrence of insulin resistance and the hepatic steatosis induced by high-fat diet, at least in part by inhibiting the expression and activity of the hepatic GSK3β.

关 键 词：胰岛素抗药性 肝脂肪变 黄芪多糖 

分 类 号：R363[医药卫生—病理学]