Schade D S, Eaton R P
Diabetes. 1975 May;24(5):510-5. doi: 10.2337/diab.24.5.510.
The potential role of glucagon in the pathogenesis of diabetic ketogenesis was examined by intravenous glucagon administration (1.0 mug/kg. body weight) in five insulin-dificient diabetic subjects. The metabolic response was defined by examining the changes in the plasma concentration of insulin, glucose, free fatty acids (FFA), triglycerides, betahydroxybutyrate, and acetoacetate in comparison to those changes occuring in five nondiabetic control subjects tested under identical experimental conditions. Our results demonstrate that in the absence of endogenous insulin secretion, exogenous glucagon administration results in an enhanced ketonemia indipendent of the rise of FFA substrate. This augmented ketogenic response to glucagon in diabetic subjects was not reflected in the dynamics of glucose regulation, with similar changes in blood glucose concentration occurring in both diabetic and nondiabetic populations. These data demonstrate that glucagon may potentiate ketonemia in insulin-deficient diabetics, although the mechanism mediating this augmentation is not defined. Since the rise in FFA substrate was indistinguishable in the diabetic as compared to the control group, increased hepatic conversion of FFA substrate into ketone bodies is suggested.
通过对五名胰岛素缺乏型糖尿病患者静脉注射胰高血糖素（1.0微克/千克体重），研究了胰高血糖素在糖尿病酮症发生机制中的潜在作用。通过检测五名非糖尿病对照受试者在相同实验条件下胰岛素、葡萄糖、游离脂肪酸（FFA）、甘油三酯、β-羟基丁酸和乙酰乙酸的血浆浓度变化，并与糖尿病患者的变化进行比较，来确定代谢反应。我们的结果表明，在缺乏内源性胰岛素分泌的情况下，外源性胰高血糖素给药会导致酮血症增强，且与FFA底物升高无关。糖尿病患者对胰高血糖素的这种增强的生酮反应并未反映在血糖调节动态中，糖尿病和非糖尿病人群的血糖浓度变化相似。这些数据表明，胰高血糖素可能会增强胰岛素缺乏型糖尿病患者的酮血症，尽管介导这种增强的机制尚不清楚。由于糖尿病组与对照组相比，FFA底物的升高没有差异，提示肝脏将FFA底物转化为酮体的能力增强。
