肝源性糖尿病发病机制的探讨  

Investigation of the pathogenesis of hepatogenic diabetes

作　　者：谭斌[1] 何伟锋[1] 温帆渊[1] 

机构地区：[1]广东省惠州市中心人民医院消化内科肝病区,广东惠州516001

出　　处：《中国医师进修杂志（内科版）》2008年第12期10-12,共3页Chinese Journal of Postgraduates of Medicine

摘　　要：目的探讨肝源性糖尿病的发病机制。方法对135例肝硬化患者分别进行空腹血糖、餐后2h血糖、血清空腹胰岛素、谷氨酸脱羧酶抗体、胰岛素释放指数及胰岛素敏感指数测定，并进行比较分析。结果肝硬化肝源性糖尿病的发生率为39.3％（53／135），其中，丙型肝炎后肝硬化肝源性糖尿病发生率53.3％（16／30），较乙型肝炎后肝硬化（37.1％，26/70）和酒精性肝硬化（31.4％，11／35）明显升高，差异有统计学意义（P〈0.01）。肝源性糖尿病患者空腹胰岛素、胰岛素释放指数、谷氨酸脱羧酶抗体阳性率均显著高于健康体检者（P〈0.01），而胰岛素敏感指数显著低于健康体检者（P〈0.01）。结论肝源性糖尿病的发生与肝硬化病因有关。除肝功能损害、胰岛素抵抗、病毒感染、免疫功能紊乱等导致胰岛β细胞功能的损伤外，胰岛素分泌相对或绝对缺乏亦是肝源性糖尿病发生的重要影响因素。Objective To investigate the pathogenesis of hepatogenic diabetes. Methods The fasting and 2-hour postprandial plasma glucose, fasting serum insulin, glutamate decarboxylase antibody, in- sulin release index （IRI） and insulin sensitivity index （ISI） was determined and analyzed in 135 liver cirrhosis patients. Results The incidence of hepatogenic diabetes was 39.3 % （53/135）in liver cirrhosis pa- tients. The incidence of hepatogenic diabetes in post hepatitis C liver cirrhosis patients （53.3%, 16/30）was much higher than that in post hepatitis B liver cirrhosis patients （37.1%, 26/70）and alcoholic liver cirrhosis patients（31.4%, 11/35）（P〈0.01 ）. The fasting serum insulin, IRI and the positivity rate of glutamate decar-boxylase antibody was much higher in hepatogenic diabetes than that in controls （P 〈 0.01 ）, and ISI was much lower than that in controls （P 〈 0.01 ）. Conclusions The development of hepatogenic diabetics is related with the etiological factor of liver cirrhosis. Besides impairment of the hepatocellular function and insulin resistance, viral infection and immunologic derangement and so on results in impairment of beta cell of islet function. Relative or absolute deficiency of insulin secretion is an important influential factor in the development of hepatogenic diabetics.

关 键 词：肝源性糖尿病 胰岛素抵抗 谷氨酸脱羧酶抗体 

分 类 号：R587.1[医药卫生—内分泌] R363.14[医药卫生—内科学]