Barrett E J, Ferrannini E, Gusberg R, Bevilacqua S, DeFronzo R A
Metabolism. 1985 May;34(5):410-20. doi: 10.1016/0026-0495(85)90205-7.
In awake dogs we measured the glucose balance across the liver and extrahepatic splanchnic tissues in the postabsorptive state and during two hours of IV infusion of glucose or for three hours following ingestion of oral glucose and during four hours of sequential intraportal followed by oral glucose. The IV glucose infusion rate was adjusted to maintain a steady state glucose concentration of either euglycemic levels (insulin clamp, group 1, N = 4), 125 mg/100 mL above the postabsorptive glucose concentration (+125 mg glucose clamp, group 2, N = 3) or 200 mg/100 mL above basal glucose levels (+200 mg glucose clamp, group 3, N = 7). Oral glucose was given at a dose of either 1.5 g/kg (group 4, N = 7) or 2.5 g/kg (group 5, N = 12). In dogs that received IV glucose, basal gut glucose uptake (0.5 +/- 0.1 mg/min X kg) was stimulated by hyperglycemia (1.5 +/- 0.5 and 1.4 +/- 0.1 mg/min X kg for group 2 and 3, respectively, P less than 0.05). In these same animals basal hepatic glucose output (-2.7 +/- 0.3 mg/min X kg) was promptly suppressed and net hepatic glucose uptake occurred (2.8 +/- 0.2 and 2.4 +/- 0.5 mg/min X kg in group 2 and 3 respectively). Euglycemic hyperinsulinemia (group 1) suppressed postabsorptive hepatic glucose release but did not enhance glucose removal by either the liver or gut tissues. After oral glucose gut tissues released absorbed glucose into portal blood. Over three hours following the glucose meal 74% and 59% of the ingested glucose was absorbed in group 4 and 5, respectively. As with IV glucose, postabsorptive hepatic glucose production was suppressed and over the first two hours after feeding the liver took up glucose (3.4 +/- 1.0 and 3.1 +/- 0.7 mg/min X kg groups 4 and 5, respectively) at a rate similar to that seen with IV glucose. To further examine the effect of the route of glucose administration on liver glucose handling, hepatic glucose balance was measured serially over four hours in three dogs that received IV glucose into a mesenteric vein to produce portal hyperglycemia (+125 mg/dL portal glucose clamp N = 3). Oral glucose (2.5 mg/kg) was given at two hours, and the rate of the mesenteric glucose infusion adjusted to maintain portal glycemia constant. The hepatic glucose balance averaged 5.5 mg/min X kg over the 0 to 2 hour period and 4.2 +/- 1.0 mg/min X kg over the 2 to 4 hour time.(ABSTRACT TRUNCATED AT 400 WORDS)
在清醒犬中,我们测量了处于吸收后状态时以及静脉输注葡萄糖两小时期间、口服葡萄糖后三小时期间和先经门静脉然后口服葡萄糖四小时期间肝脏和肝外内脏组织的葡萄糖平衡。调整静脉葡萄糖输注速率以维持血糖水平处于正常血糖水平(胰岛素钳夹法,第1组,N = 4)、比吸收后血糖浓度高125 mg/100 mL(+125 mg葡萄糖钳夹法,第2组,N = 3)或比基础血糖水平高200 mg/100 mL(+200 mg葡萄糖钳夹法,第3组,N = 7)的稳态。口服葡萄糖的剂量为1.5 g/kg(第4组,N = 7)或2.5 g/kg(第5组,N = 12)。在接受静脉葡萄糖的犬中,基础肠道葡萄糖摄取(0.5±0.1 mg/min·kg)受到高血糖刺激(第2组和第3组分别为1.5±0.5和1.4±0.1 mg/min·kg,P<0.05)。在这些相同的动物中,基础肝脏葡萄糖输出(-2.7±0.3 mg/min·kg)迅速受到抑制,肝脏出现净葡萄糖摄取(第2组和第3组分别为