摘要
采用小剂量注射链脲佐菌素联合高脂高糖饮食建立糖尿病大鼠模型,并灌胃给予桑叶多糖MLPⅡ,用电子显微镜观察各试验组大鼠肝脏组织超微结构变化,采用Western blot与RT-PCR方法分别检测大鼠肝脏组织的葡萄糖激酶(glucokinase,GCK)和胰岛素受体底物2(insulin receptor substrate 2,IRS-2)的蛋白质表达水平以及基因mRNA转录水平,研究桑叶多糖MLPⅡ的降血糖作用机制。结果表明:与糖尿病模型对照组相比,150 mg/kg桑叶多糖MLPⅡ治疗组大鼠肝脏细胞超微结构得到明显改善,肝糖原颗粒明显增多,GCK和IRS-2的蛋白质表达水平及基因mRNA转录水平显著上升(P<0.05)。结果提示,桑叶多糖MLPⅡ能显著调节糖尿病模型大鼠的糖代谢,其作用机制可能与改善糖尿病模型大鼠肝脏细胞超微结构,上调IRS-2介导的GCK表达,促进肝糖原合成与贮存有关。
In this study, low dose injection of streptozotocin and high-fat high-sugar diet were jointly applied to estab- lish rat models with diabetes mellitus. After the model rats were gavaged with mulberry leaf polysaccharide MLP Ⅱ , the hypoglycemic mechanism of mulberry leaf polysaccharide MLP Ⅱ was investigated through observing ultrastructural changes in liver tissues of the diabetic model rats in each experimental group by electron microscope and measuring the protein expression and gene mRNA transcription levels of glucokinase （GCK） and insulin receptor substrate 2 （IRS-2） in liver tissues of the diabetic model rats by Western blotting and RT-PCR respectively. The results showed that, compared with the diabetic control group, the ultrastructure of hepatic cells of diabetic model rats in the 150 mg/kg MLP Ⅱ-treated group was improved remarkably, the amount of hepatic glycogen particles was increased obvi- ously, and the protein expression and gene mRNA transcription levels of GCK and IRS-2 increased significantly （ P 〈0. 05）. These results demonstrated that mulberry leaf polysaccharide MLP Ⅱ could remarkably regulate glyco- me-tabolism of diabetic model rats and the regulatory mechanism may be associated with improving the ultra- structure of hepatic cells, promoting the expression of GCK mediated by IRS-2, and stimulating the synthesis and storage of hepatic glycogen.
出处
《蚕业科学》
CAS
CSCD
北大核心
2013年第5期967-972,共6页
ACTA SERICOLOGICA SINICA
基金
中国博士后科学基金项目(No.2013M531641)
现代农业产业技术体系专项(No.CARS-22)
关键词
桑叶多糖
糖尿病模型大鼠
肝脏
糖代谢
葡萄糖激酶
Mulberry leaf polysaccharide
Diabetic mod-el rat
Liver
Glycometabolism
Glucokinase
