肝源性糖尿病发病机制的探讨

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),而胰岛索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.

Investigation of the pathogenesis of hepatogenic diabetes

Objective To investigate the pathogenesis of hepatogenic diabetes.Methods The fasting and 2-hour postprandial plasma glucose,fasting sertum insulin,glutamate decarboxylase antibody,insulin release index (IRI)and insulin sensitivity index(ISI)Was determined and analyzed in 135 liver cirrhosis patients.Results The incidence of hepatogenic diabetes wag 39.3%(53/135)in liver cirrhosis patients.The incidence of hepatogenic diabetes in post hepatitis C liver cirrhosis patients(53.3%.16/30)was muchh igher than that in post hepatitis B liver cirrhosis patients(37.1%,26/70)and alcohofic liver cirrhosis patients(31.4%.11/35)(P＜0.01).The fasting serum insulin,IRI and the positivity rate of glutamate decarboxylase antibody was much higher in hepatogenic diabetes than that in controls(P＜0.01),and ISl was much lower than that in controls(P＜0.01).Conclusions The development of hepatogenic diabetics is relsted 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.