Bergman R N, Beir J R, Hourigan P M
Diabetes. 1982 Jan;31(1):27-35. doi: 10.2337/diab.31.1.27.
These studies were designed to test whether a putative gastrointestinal factor (separate from that stimulating insulin release) is involved in the enhancement of liver glycogen storage during oral glucose ingestion. To do this, we compared net hepatic glucose uptake in conscious dogs, following oral glucose administration, with hepatic uptake during intraportal glucose infusion. The rate of intraportal glucose infusion was calculated to match the time course of gut glucose absorption in the oral administration experiments. In control studies, intragastric instillation of tap water [90 +/- 2.4 (SE) in four dogs had no effect on basal rates of gastrointestinal (GI) glucose uptake (16 +/- 1 mg/min) oe hepatic glucose production (97 +/- 3 mq/min). Net basal GI lactate production was equal to GI glucose utilization (P greater than 0.1); glycolytic conversion of glucose to lactate accounted for all basal GI glucose utilization. In oral experiments, gastric instillation of 1.2 g/kg glucose (N = 8) caused GI glucose absorption to increase within 5 min (P less than 0.01). Net glucose absorption from the gut was maximal (355 1.55 mg/min) at 60 min, and was complete at 165-240 min (mean = 186 min). During absorption, liver switched from production to net uptake by 30 min (P less than 0.01); production was resumed by 3 h. Total glucose taken up by liver was 7.19 +/- 1.8 g (23% oral load). No net metabolism of the instilled glucose to lactate occurred during absorption; GI lactate production was the same during absorption (13.0 +/- 5.0 mg/min) as before glucose instillation (11.2 +/- 2.0 mg/min; P greater than 0.45). In intraportal experiments, intraportal glucose infusion (total = 1.09 g/kg) induced liver to take up glucose by 15 min (P less than 0.01); total hepatic uptake (4.6 +/- 1.5 g) was not significantly different from the oral experiments (P greater than 0.15). Also, nonsplanchnic glucose uptake was the same in the oral (25.1 +/- 2.2) and intraportal (25.2 +/- 1.4) studies. The lack of difference between hepatic and extrahepatic fates of administered glucose with oral and intraportal administration indicates that no putative gut factor need be invoked to explain hepatic glycogen deposition during oral glucose, and it seems probable that no such factor exists in the dog.
这些研究旨在测试一种假定的胃肠因子（与刺激胰岛素释放的因子不同）是否参与口服葡萄糖期间肝脏糖原储存的增强。为此，我们比较了清醒犬口服葡萄糖后肝脏的净葡萄糖摄取与门静脉内输注葡萄糖期间的肝脏摄取。门静脉内葡萄糖输注速率的计算方式是使其与口服给药实验中肠道葡萄糖吸收的时间进程相匹配。在对照研究中，向四只犬胃内滴注自来水[90±2.4（标准误）]对胃肠道（GI）葡萄糖摄取的基础速率（16±1毫克/分钟）或肝脏葡萄糖生成（97±3毫克/分钟）没有影响。基础GI乳酸生成量等于GI葡萄糖利用率（P＞0.1）；葡萄糖糖酵解转化为乳酸占所有基础GI葡萄糖利用率。在口服实验中，向胃内滴注1.2克/千克葡萄糖（N = 8）导致GI葡萄糖吸收在5分钟内增加（P＜0.01）。肠道净葡萄糖吸收在60分钟时达到最大值（355±1.55毫克/分钟），并在165 - 240分钟（平均 = 186分钟）时完成。在吸收过程中，肝脏在30分钟时从葡萄糖生成转变为净摄取（P＜0.01）；3小时后恢复生成。肝脏摄取的葡萄糖总量为7.19±1.8克（占口服负荷的23%）。在吸收过程中，注入的葡萄糖没有净代谢为乳酸；吸收期间GI乳酸生成与滴注葡萄糖前相同（13.0±5.0毫克/分钟）（11.2±2.0毫克/分钟；P＞0.45）。在门静脉内实验中，门静脉内输注葡萄糖（总量 = 1.09克/千克）在15分钟时诱导肝脏摄取葡萄糖（P＜0.01）；肝脏总摄取量（4.6±1.5克）与口服实验无显著差异（P＞0.15）。此外，口服（25.1±2.2）和门静脉内（25.2±1.4）研究中的非内脏葡萄糖摄取相同。口服和门静脉内给药后肝脏和肝脏外葡萄糖去向缺乏差异表明，无需调用假定的肠道因子来解释口服葡萄糖期间肝脏糖原沉积，而且犬体内似乎不存在这样的因子。
