Interaction of Insulin and Prior Exercise in Control of Hepatic Metabolism of a Glucose Load

Abstract

To determine if prior exercise enhances insulin-stimulated extraction of glucose by the liver, chronically catheterized dogs were submitted to 150 min of treadmill exercise or rest. After exercise or rest, dogs received portal glucose (18 μmol · kg−1 · min−1), peripheral somatostatin, and basal portal glucagon infusions from t = 0 to 150 min. A peripheral glucose infusion was used to clamp arterial blood glucose at 8.3 mmol/l. Insulin was infused into the portal vein to create either basal levels or mild hyperinsulinemia. Prior exercise did not increase whole-body glucose disposal in the presence of basal insulin (25.5 ± 1.5 vs. 20.3 ± 1.7 μmol · kg−1 · min−1), but resulted in a marked enhancement in the presence of elevated insulin (97.2 ± 15.1 vs. 64.4 ± 7.4 μmol · kg−1 · min−1). Prior exercise also increased net hepatic glucose uptake in the presence of both basal insulin (7.5 ± 1.2 vs. 2.9 ± 2.4 μmol · kg−1 · min−1) and elevated insulin (22.0 ± 3.5 vs. 11.5 ± 1.8 μmol · kg−1 · min−1). Likewise, net hepatic glucose fractional extraction was increased by prior exercise with both basal insulin (0.04 ± 0.01 vs. 0.01 ± 0.01 μmol · kg−1 · min−1) and elevated insulin (0.10 ± 0.01 vs. 0.05 ± 0.01). Hepatic glycogen synthesis was increased by elevated insulin, but was not enhanced by prior exercise. Although the increase in glucose extraction after exercise could be ascribed to increased insulin action, the increase in hepatic glycogen synthesis was independent of it.