兰州大学机构库 >生命科学学院
地黄寡糖降血糖作用机制研究-对肝糖代谢及相关基因表达的影响
Alternative TitleThe mechanism of hypoglycemic effect of Rehmannia glutinosa oligosaccharides:the influence on the hepatic glucose metabolism and the related gene expression
刘景龙
Thesis Advisor贾正平 ; 张汝学
2009-05-25
Degree Grantor兰州大学
Place of Conferral兰州
Degree Name硕士
Keyword地黄寡糖 2型糖尿病 胰岛素抵抗 降血糖 肝脏 关键酶 分子机制
Abstract中 文 摘 要 目 的 1. 研究地黄寡糖在2型糖尿病大鼠模型和高脂饲料加地塞米松(DEX)联合诱导的胰岛素抵抗大鼠模型上对肝糖代谢关键酶及相关基因表达的影响。 2. 研究地黄寡糖在高脂诱导的胰岛素抵抗大鼠模型上对糖代谢的改善作用及相关机制。 方 法 1. 采用长期高脂肪饲料饲养加小剂量链脲佐菌素(STZ,30 mg•kg-1,i.p.)联合诱导大鼠2型糖尿病大鼠模型。大鼠分为正常对照组、2型糖尿病模型组、ROS(100、200 mg•kg-1•d-1)给药组及阳性对照二甲双胍(200 mg•kg-1•d-1)给药组,以上各组均为灌胃给药。从体重、空腹血糖、饮水量、摄食量、肌糖原含量及脏器指数等方面考查地黄寡糖对2型糖尿病大鼠糖代谢的改善作用。 2. 研究地黄寡糖对2型糖尿病大鼠肝糖代谢关键酶活性及基因表达的影响。取肝脏研究ROS对肝糖原含量及肝脏葡萄糖激酶及葡糖糖-6-磷酸酶活性以及基因表达的影响。取大鼠肌肉组织研究地黄寡糖对GLUT4基因表达的影响,取脂肪组织研究地黄寡糖对脂联素、TNF-α和PPAR-γ基因表达的影响。 3. 采用高脂饲料加DEX(1 mg•kg-1)隔日腹腔注射联合诱导胰岛素抵抗大鼠模型。大鼠分为正常对照组、胰岛素抵抗模型组、ROS给药组(100, 200 mg•kg-1•d-1,i.g.)及阳性对照罗格列酮组(3.4 mg•kg-1•d-1,i.g.),以上各组均为灌胃给药。给药期间隔周测定大鼠糖耐量,给药第6周处死大鼠。从糖耐量、体重及脏器指数等方面考查地黄寡糖对胰岛素抵抗大鼠胰岛素抵抗的改善作用。 4. 研究地黄寡糖对胰岛素抵抗大鼠肝糖代谢关键酶活性及基因表达的影响。取肝脏研究ROS对肝糖原含量及肝脏葡萄糖激酶及葡萄糖-6-磷酸酶活性以及基因表达的影响。取大鼠肌肉组织研究地黄寡糖对GLUT4基因表达的影响,取脂肪组织研究地黄寡糖对脂联素、TNF-α和PPAR-γ基因表达的影响。 5. 研究地黄寡糖在高脂胰岛素抵抗大鼠模型上对胰岛素抵抗的改善作用及机制。高脂肪饲料饲养2个月诱导高脂胰岛素抵抗大鼠模型。大鼠随机分为正常对照组、胰岛素抵抗模型组、ROS给药组(100、200 mg•kg-1•d-1)及二甲双胍给药组(200 mg•kg-1•d-1),以上各组均为灌胃给药。给药期间隔周测定大鼠糖耐量,给药第6周处死大鼠。从糖耐量、体重、血脂、糖原含量、脏器指数和肌肉HK活性等方面考查地黄寡糖对高脂胰岛素抵抗大鼠胰岛素抵抗的改善作用及机制。 结 果 1. ROS在2型糖尿病大鼠模型上的降血糖作用及机制。ROS可降低2型糖尿病大鼠的空腹血糖值(P<0.05);使2型糖尿病大鼠体重增加;可以显著降低2型糖尿病大鼠摄食量(P<0.05)和饮水量(P<0.01);ROS对2型糖尿病大鼠脏器指数也有一定改善作用。机制方面,地黄寡糖能够显著增加2型糖尿病大鼠肝糖原含量(P<0.01),提高GK活性(P<0.01)和基因表达量(P<0.05),减少G-6-Pase活性(P<0.01)和基因表达量(P<0.05);地黄寡糖能够显著增加PPAR-γ(P<0.05)、脂联素(P<0.01)和GLUT4基因表达量(P<0.05)。 2. ROS在地塞米松诱导的胰岛素抵抗大鼠模型上对胰岛素抵抗的改善...
Other AbstractAbstract Objective: 1. To study the effect of Rehmannia glutinosa oligosaccharides (ROS) on the key enzymes of the hepatic glucose metabolism and the related gene expression in type 2 diabetic and dexamethasone- induced insulin resistant rats. 2. To study the ameliorative effect and mechanism of ROS on the glucose metabolism in high lipid food -induced insulin resistant rats. Methods: 1. To induce the model of type 2 diabetic rats which were injected intraperitoneally with STZ (30 mg•kg-1) after fed with high lipid food for two months. The rats were divided into the control group, type 2 diabetic model group, ROS (100, 200 mg•kg-1•d-1) treated group and metformin (200 mg•kg-1•d-1) treated group. All drugs were administered by intragastric administration (i.g.). The ameliorative effects of ROS on glucose metabolism in type 2 diabetic rats were evaluated through the changes of the body weight, plasma glucose, quantity of ingestion, quantity of drinking, content of the hepatic glycogen, content of the muscle glycogen and index of organs. 2. Studying the effect of ROS on the activity and gene expression of hepatic key enzymes in type 2 diabetic rats.Taking the liver to determine the activity and gene expression of GK and G-6-Pase, the skeletal muscle to determine the gene expression of GLUT4 and the fat to determine the gene expression of TNF-α, PPAR-γ and adiponectin by RT-PCR. 3. The insulin resistance model was induced by both high lipid food and dexamethasone (1 mg•kg-1, i.p. every other day).The rats were divided into the control group, insulin resistance model group, ROS (100,200 mg•kg-1•d-1) treated group and rosiglitazone (3.4 mg•kg-1•d-1) treated group. All drugs were administered by intragastric administration (i.g.). The glucose tolerance test was taken every other week. The rats were killed after they had been administered for six weeks. The ameliorative effects of ROS on insulin resistance were measured through the glucose tolerance, body weight and organ index. 4. Studying the effect of ROS on the activity and gene expression of hepatic key enzymes indexamethasone-induced insulin resistant rats.Taking the liver to determine the activity and gene expression of GK and G-6-Pase, the skeletal muscle to determine the gene expression of GLUT4, the fat to determine the gene expression of TNF-α, PPAR-γ and adiponectin by RT-PCR. 5. Studying the ameliorative effect and mechanism of RO...
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Language中文
Document Type学位论文
Identifierhttps://ir.lzu.edu.cn/handle/262010/221551
Collection生命科学学院
Recommended Citation
GB/T 7714
刘景龙. 地黄寡糖降血糖作用机制研究-对肝糖代谢及相关基因表达的影响[D]. 兰州. 兰州大学,2009.
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