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) ml] 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 > 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 < 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 < 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 > 0.45). In intraportal experiments, intraportal glucose infusion (total = 1.09 g/kg) induced liver to take up glucose by 15 min (P < 0.01); total hepatic uptake (4.6 ± 1.5 g) was not significantly different from the oral experiments (P > 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.

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