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机构地区:[1]武汉大学人民医院内分泌科,湖北武汉430060
出 处:《中国病理生理杂志》2004年第10期1866-1870,共5页Chinese Journal of Pathophysiology
摘 要:目的 :检测骨骼肌细胞膜GLUT4含量的改变 ,探讨高脂饮食喂养诱导胰岛素抵抗的受体后机制。方法 :将动物分为 3组 :①正常对照组 ;②高脂饮食组 ;③高脂饮食 +饮食控制组。通过 8周高脂饮食喂养建立胰岛素抵抗大鼠模型 ,随后代以普通饮食继续喂养 4周。用Westernblot方法检测骨骼肌细胞膜表面GLUT4蛋白表达。结果 :在胰岛素刺激下 ,高脂饮食组大鼠骨骼肌细胞膜GLUT4蛋白表达显著少于正常对照组 (减少约 31% ) ;饮食控制组骨骼肌细胞膜GLUT4蛋白表达明显高于高脂饮食组 (约 1 14倍 )。结论 :高脂喂养的方法可成功复制出胰岛素抵抗大鼠模型 ;高脂饮食可能通过影响胰岛素信号转导系统 ,使胰岛素刺激的GLUT4转位至细胞膜受阻 ,其在膜上的含量也降低 。AIM: To explore the change of the amount of GLUT4 protein at the plasma membrane of the rat skeletal muscle after high-fat feeding. METHODS: The animals were divided into three groups (ten for each): group I: control; group II: high-fat feeding; group III: high-fat feeding + dietary treatment. The rat model of insulin resistance (IR) was made by feeding high-fat diet for eight weeks. And then insulin-resistant rats were fed with chow diet for 4 weeks. Fasting plasma glucose and fasting serum insulin levels were measured before and after dietary treatment, respectively. Insulin treatment was achieved by intraperitoneal injection of insulin (10 unit insulin per kg body weight) 15 minutes before killing the animals. The right hindlimb skeletal muscle was rapidly dissected. Then the expression of GLUT4 protein at the plasma membrane in all the animals was assessed with Western bloting. RESULTS: The GLUT4 content at the plasma membrane in high-fat-fed rat skeletal muscle was significantly lower (about 31%) than that in controls (P<0.01). Dietary treatment partly corrected fasting blood glucose [from (6.20±0.39) mmol/L to (5.78±0.74) mmol/L] and fasting serum insulin levels [from (17.19±1.93) mU/L to (11.68±1.28) mU/L] and increased the GLUT4 content at the plasma membrane by 1.14-fold in insulin-resistant rat skeletal muscle. CONCLUSION: High-fat feeding induces IR in Sprague-Dawley rats. The mechanism may be involved in decreased cell-surface level of GLUT4 through affecting intracellular insulin signaling and then decreasing GLUT4 trafficking. [
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