Diabetes 52:1897-1903, 2003
© 2003 by the American Diabetes Association, Inc.
Interaction of Insulin and Prior Exercise in Control of Hepatic Metabolism of a Glucose Load
R. Richard Pencek1,
Freyja James1,
D. Brooks Lacy1,
Kareem Jabbour2,
Phillip E. Williams1,
Patrick T. Fueger1, and
David H. Wasserman1,3
1 Department of Molecular Physiology & Biophysics, Vanderbilt University School of Medicine, Nashville, Tennessee
2 Department of Surgery, Vanderbilt University School of Medicine, Nashville, Tennessee
3 Diabetes Research and Training Center, Vanderbilt University School of Medicine, Nashville, Tennessee
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.
Address correspondence and reprint requests to Richard Pencek, Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, TN 37232-0615. E-mail: r.r.pencek{at}vanderbilt.edu

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Copyright © 2003 by the American Diabetes Association.
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