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Am J Physiol Endocrinol Metab 280: E918-E927, 2001;
0193-1849/01 $5.00
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Vol. 280, Issue 6, E918-E927, June 2001

Stimulation of splanchnic glucose production during exercise in humans contains a glucagon-independent component

Robert H. Coker1, Lene Simonsen3, Jens Bülow3, David H. Wasserman2, and Michael Kjær4

1 Division of Exercise Science, University of Mississippi, University, Mississippi 38677; 2 Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, Tennessee 37232; and 3 Department of Clinical Physiology and 4 Sports Medicine Research Unit, Bispebjerg Hospital, DK-2400 Copenhagen, Denmark

To determine the importance of basal glucagon to the stimulation of net splanchnic glucose output (NSGO) during exercise, seven healthy males performed cycle exercise during a pancreatic islet cell clamp. In one group (BG), glucagon was replaced at basal levels and insulin was adjusted to achieve euglycemia. In another group (GD), only insulin was replaced at the identical rate used in BG, and basal glucagon was not replaced. Exogenous glucose infusion was necessary to maintain euglycemia during exercise in BG and during rest and exercise in GD. Arterial glucagon was at least twofold greater in BG than in GD throughout the pancreatic islet cell clamp. Although basal NSGO remained stable in BG (2.5 ± 0.5 mg · kg-1 · min-1), basal NSGO dropped by 70% in GD (0.7 ± 0.3 mg · kg-1 · min-1). NSGO was also greater in BG than in GD at 10 min of moderate exercise, most likely due to the residual effect of basal glucagon replacement. However, NSGO increased slightly and remained similar throughout the remainder of moderate and heavy exercise in BG and GD. Therefore, a mechanism independent of changes in pancreatic hormones and/or the level of glycemia contributes toward modest stimulation of NSGO during moderate and heavy exercise.

islet cell clamp; hormone replacement


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