实验性非胰岛素依赖型糖尿病大鼠肝脏葡萄糖激酶活性的改变.docVIP

实验性非胰岛素依赖型糖尿病大鼠肝脏葡萄糖激酶活性的改变 实验性非胰岛素依赖型糖尿病大鼠肝脏葡萄糖激酶活性的改变 2011-07-21 马晓伟　钱荣立　王艳荣　陈澜　惠岩 　　【摘要】　目的　研究实验性非胰岛素依赖型糖尿病(NIDDM)大鼠肝脏葡萄糖激酶活性的改变。方法　选用雄性Wistar大鼠13只用半量链脲佐菌素(30 μg/g体重)加高脂、高糖、高热量饲料喂养18周，制成类非胰岛素依赖型糖尿病模型，另选用20只作为对照组，观察两组血糖和胰岛素释放水平，同时测肝脏葡萄糖激酶活性。结果　糖尿病组肝脏葡萄糖激酶活性(2.17±0.20 U/g肝组织)明显低于正常对照组(2.87±0.11 U/g肝组织，P＜0.01)。结论　肝脏葡萄糖激酶活性降低可能参与NIDDM的发病机制。 　　【关键词】　糖尿病，非胰岛素依赖型　　葡糖激酶　　胰岛素抵抗 A study on the change of liver glucokinase activity in experimental non-insulin dependent diabetes mellitus rats　　Ma Xiaowei, Qian Rongli, Wang Yanrong, et al. Department of Endocrinology, First Teaching Hospital, Beijing Medical University, Beijing 100034 　　【Abstract】　Objective　To study the change of liver glucokinase activity in the experimental non-insulin dependent diabetes mellitus (NIDDM) rats. Methods　13 male Wistar rats were injected with half of the regular dose of STZ (30 μg/g body weight) via tail vein and fed on a diet of high fat and high calorie for 18 weeks. Blood glucose and insulin concentrations were determined during experimental period. The diabetic rats were characteristic of NIDDM. Then the liver glucokinase (GK) activity was determined. Results　The liver GK activity in diabetic rats (2.17±0.20 U/g liver) was significantly lower than that in the controls (2.87±0.11 U/g liver, P0.01). Conclusion　GK is the major isoenzyme of hexokinase in rat liver, so decrease of liver GK activity may contribute to the pathogenetic mechanisms of NIDDM. 　　【Key words】　Non-insulindependentdiabetesmellitus　　Glucokinase　　Insulin resistance 　　血糖稳态是保证器官组织生理功能正常的关键，为人类长寿所必需。葡萄糖激酶(GK)［E2.7.1.2］对维持血糖稳态起着重要作用。GK是调节糖代谢的关键酶，主要存在于肝实质细胞和胰岛β细胞中，控制β细胞内葡萄糖诱导的胰岛素释放，在肝脏和胰岛β细胞中起着葡萄糖感受器和信息产生器的作用［1］。国外曾有关于链脲佐菌素(STZ)所致胰岛素依赖型糖尿病(IDDM)大鼠肝葡萄糖激酶活性改变的报道［2］。我们拟通过对类非胰岛素依赖型糖尿病动物模型研究肝GK活性的改变，以进一步在理论上从细胞酶学改变水平阐明非胰岛素依赖型糖尿病(NIDDM)糖代谢障碍的发病机制，并为临床对NIDDM的防治途径提供理论指导依据。 材料和方法 　　一、动物模型［3］ 　　雄性Wistar大鼠(本院动物实验中心提供)若干只，体重230～250 g，随机分成两组，一组由尾静脉注射30 μg/g体重链脲佐菌素(STZ，美国Sigma公司提供)。2～3周后测糖耐量，选异常者13只加喂高脂、高糖、高热量饲料(22%脂肪，52%蔗糖，18%蛋白质及适量