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研究利用含 2 0 %猪油的高脂饲料诱发大鼠肥胖模型 ,对胰岛素在肥胖发生中的作用 ,及胰岛素受体酪氨酸蛋白激酶活性的变化进行研究 ,并探讨耐力运动的减体脂机制 ,及饮食脂肪含量对胰岛素受体酶活性的影响。得出以下结论 :1.高脂饲料诱发肥胖鼠存在高胰岛素血症 ,胰岛素敏感性下降 ,及胰岛素抵抗。其肝细胞膜、脂肪细胞膜、肌细胞膜胰岛素受体结合容量下降 ,同时 ,肝细胞膜与肌细胞膜胰岛素受体酪氨酸激酶活性 (受体激酶自动磷酸化 )也下降 ,加重了胰岛素抵抗程度。 2 .耐力运动可减少高脂饲料诱发肥胖鼠体脂含量 ,通过增加肥胖鼠细胞膜胰岛素受体结合力 ,减轻其胰岛素抵抗。减少饮食中脂肪含量同时结合耐力运动 ,可降低肥胖鼠的体脂含量至对照水平 ,既可提高细胞膜胰岛素受体结合力 ,也可提高受体后 TPK活性 ,使肥胖鼠的胰岛素抵抗得到最好的改善
To study the use of high fat diet containing 20% lard induced rat obesity model, the role of insulin in the occurrence of obesity, and changes in insulin receptor tyrosine protein kinase activity, and to study the endurance exercise reduced fat Mechanism, and dietary fat content on insulin receptor enzyme activity. Draw the following conclusions: 1.High fat diet induced obesity in rats with hyperinsulinemia, decreased insulin sensitivity, and insulin resistance. The hepatic cell membrane, fat cell membrane, muscle cell membrane insulin receptor binding capacity decreased at the same time, the liver cell membrane and muscle cell membrane insulin receptor tyrosine kinase activity (receptor kinase autophosphorylation) also decreased, increasing the degree of insulin resistance. Endurance exercise can reduce the body fat content of obese rats induced by high fat diet, and reduce the insulin resistance by increasing the insulin receptor binding ability of obese rat plasma membrane. Reduce the fat content of the diet combined with endurance exercise can reduce body fat content of obese rats to the control level, can improve the binding capacity of the cell membrane insulin receptor, but also increase the receptor TPK activity, so that obese mice insulin resistance is best Improvement