Influence of hyperinsulinemia, hyperglycemia, and the route of glucose administration on splanchnic glucose exchange

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Abstract
The effects of hyperinsulinemia, hyperglycemia and the route of glucose administration on total glucose utilization and on net splanchnic glucose exchange were studied in 20 normal volunteers with the hepatic venous catheter technique. Euglycemic hyperinsulinemia [induced by a priming plus continuous infusion of insulin resulting in plasma insulin levels of 400-1200 .mu.IU/ml and a variable glucose infusion] caused a 5 to 6-fold increase above basal in total glucose turnover. However, net splanchnic glucose uptake (0.5 .+-. 0.2 mg/kg per min) accounted for only 4-5% of total glucose utilization. When hyperglycemia (223 .+-. 1 mg/dl) was induced in addition to hyperinsulinemia by i.v. glucose infusion, splanchnic glucose uptake increased 100% to 1.0-1.1 mg/kg per min but was still responsible for only 10-14% of total glucose utilization. In other studies hyperglycemia (223 .+-. 2 mg/dl) was maintained constant by a variable i.v. infusion of glucose for 4 h and oral glucose (1.2 mg/kg) was administered at 1 h. After the oral glucose, net splanchnic glucose uptake increased to values 6-fold higher than with i.v. glucose despite unchanged plasma glucose levels and plasma insulin concentrations well below those observed in the studies with euglycemic hyperinsulinemia. Hyperinsulinemia or hyperglycemia induced by i.v. infusion of glucose or insulin apparently causes minimal net glucose uptake by the splanchnic bed despite marked stimulation of total glucose turnover. Glucose administration per os has a marked stimulatory effect on net splanchnic glucose uptake. Orally consumed glucose may cause the release of a gastrointestinal factor that enhances insulin-mediated glucose uptake by the liver.