Clore J N, Blackard W G
Division of Endocrinology, Diabetes and Metabolism, Medical College of Virginia, Virginia Commonwealth University, Richmond 23298-0111.
Diabetes. 1994 Feb;43(2):256-62. doi: 10.2337/diab.43.2.256.
To determine the effect of inhibition of gluconeogenesis on liver glycogen stores in patients with non-insulin-dependent diabetes mellitus (NIDDM) after a 3-day fast, 10% ethanol (EtOH) was administered intravenously to nine obese patients with NIDDM and six obese nondiabetic subjects. Rates of glucose appearance (3-[3H]glucose) and [U-14C]alanine incorporation into glucose (alanine gluconeogenesis [Ala-GNG]) were determined before and during EtOH administration, and residual glycogen stores were assessed by the incremental glucose response to glucagon (glucoseAUC). Hepatic glucose output (HGO) was closely correlated with plasma glucose levels (r = 0.71, P < 0.001) after the 3-day fast and was significantly greater in the diabetic compared with the nondiabetic subjects (13.8 +/- 1.4 vs. 7.6 +/- 0.6 mumol.kg-1 FFM.min-1, P < 0.01). During the 120-min EtOH infusion, Ala-GNG fell by more than 50% in both groups and did not increase after intravenous glucagon administration. HGO fell modestly in both the diabetic and nondiabetic subjects during the first 30 min of EtOH infusion and stabilized thereafter. In contrast to Ala-GNG, HGO increased significantly after intravenous glucagon administration in both the diabetic and nondiabetic subjects, but the increase was significantly greater in the patients with NIDDM (P < 0.01). The glucose area under the curve in response to glucagon (glucoseAUC) was lower in the presence of EtOH than in its absence (14.9 +/- 7 vs. 68 +/- 15.6 mM/min, P < 0.01) in the obese nondiabetic subjects, which suggests a decrease in liver glycogen stores.(ABSTRACT TRUNCATED AT 250 WORDS)
为了确定抑制糖异生对非胰岛素依赖型糖尿病（NIDDM）患者禁食3天后肝脏糖原储备的影响，对9名肥胖的NIDDM患者和6名肥胖的非糖尿病受试者静脉注射10%乙醇（EtOH）。在注射EtOH之前和期间，测定葡萄糖生成率（3-[3H]葡萄糖）以及[U-14C]丙氨酸转化为葡萄糖的速率（丙氨酸糖异生[Ala-GNG]），并通过胰高血糖素刺激后的葡萄糖增量反应（葡萄糖AUC）评估残余糖原储备。禁食3天后，肝葡萄糖输出（HGO）与血浆葡萄糖水平密切相关（r = 0.71，P < 0.001），糖尿病患者的HGO显著高于非糖尿病受试者（13.8±1.4对7.6±0.6 μmol·kg-1去脂体重·min-1，P < 0.01）。在120分钟的EtOH输注过程中，两组的Ala-GNG均下降超过50%，静脉注射胰高血糖素后未增加。在EtOH输注的前30分钟，糖尿病和非糖尿病受试者的HGO均略有下降，此后稳定。与Ala-GNG不同，糖尿病和非糖尿病受试者静脉注射胰高血糖素后HGO均显著增加，但NIDDM患者的增加幅度更大（P < 0.01）。在肥胖的非糖尿病受试者中，存在EtOH时胰高血糖素刺激后的葡萄糖曲线下面积（葡萄糖AUC）低于不存在EtOH时（14.9±7对68±15.6 mM/min，P < 0.01），这表明肝脏糖原储备减少。（摘要截短至250字）
