Adlung J, Kelch L, Peters J, Grazikowske H
Z Gastroenterol. 1977 Sep;15(9):553-64.
In 21 patients with liver cirrhosis, 35 normal subjects, 8 patients with chemical and 11 with manifest diabetes 0.5 g glucose/kg together with 14C-glucose were injected intravenously. 71% of the cirrhotics showed an impaired glucose tolerance. IRI response was exaggerated. The insulinogenic index was elevated in patients with liver cirrhosis and normal glucose tolerance and normal or subnormal in those with carbohydrate intolerance, as well as in diabetics. Decrease of the specific activity of glucose, expressing supply of non-labelled glucose to the body pool, was much more rapid in patients with carbohydrate intolerance, either hepatogenic or not, when compared at equal glucose concentrations. Moreover all groups with deteriorated glucose tolerance exhaled less 14CO2. Consequently, diabetes in chronic liver disease displays the same abnormalities as diabetes in obesity with respect to liver glucose supply and glucose oxidation. In both conditions diminished glucose assimilation is usually the result of reduced removal and increased supply. Therefore it is concluded that impaired hepatic uptake of glucose cannot be implicated as a single cause of hepatogenic diabetes.
对21例肝硬化患者、35名正常受试者、8例化学性糖尿病患者和11例显性糖尿病患者静脉注射0.5g葡萄糖/千克体重以及14C标记的葡萄糖。71%的肝硬化患者糖耐量受损。胰岛素释放指数反应过度。肝硬化且糖耐量正常患者的胰岛素生成指数升高,而糖耐量异常患者以及糖尿病患者的胰岛素生成指数正常或低于正常水平。在相同葡萄糖浓度下比较时,无论是肝源性还是非肝源性糖耐量异常患者,代表非标记葡萄糖向体内池供应的葡萄糖比活性下降更快。此外,所有糖耐量恶化的组呼出的14CO2都较少。因此,就肝脏葡萄糖供应和葡萄糖氧化而言,慢性肝病中的糖尿病与肥胖症中的糖尿病表现出相同的异常。在这两种情况下,葡萄糖同化减少通常是清除减少和供应增加的结果。因此得出结论,肝脏对葡萄糖摄取受损不能被认为是肝源性糖尿病的唯一原因。