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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
http://www.100md.com 《中华内科杂志》 1998年第2期
     马晓伟 钱荣立 王艳荣 陈澜 惠岩 100034 北京医科大学第一医院内分泌科 中华内科杂志 1998 0 37 2


    关键词: 期刊 zhnkzz 0 糖尿病,非胰岛素依赖型葡糖激酶胰岛素抵抗 fur -->


    

【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。

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 T o 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 μ g/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, P<0.01). 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 ......


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