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Am J Physiol Endocrinol Metab 273: E972-E980, 1997;
0193-1849/97 $5.00
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Vol. 273, Issue 5, E972-E980, November 1997

Interaction of equal increments in arterial and portal vein insulin on hepatic glucose production in the dog

Dana K. Sindelar, Chang A. Chu, Doss W. Neal, and Alan D. Cherrington

Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, Tennessee 37232-0615

We have previously shown that a selective increase of 84 pmol/l in either arterial or portal vein insulin (independent of a change in insulin in the other vessel) can suppress tracer-determined glucose production (TDGP) and net hepatic glucose output (NHGO) by ~50%. In the present study we investigated the interaction between equal increments in arterial and portal vein insulin in the suppression of TDGP and NHGO. Isotopic ([3-3H]glucose) and arteriovenous difference methods were used in conscious overnight fasted dogs. A pancreatic clamp was used to control the endocrine pancreas. A 40-min basal period was followed by a 180-min test period, during which arterial and portal vein insulin levels were simultaneously and equally increased 102 pmol/l. Hepatic sinusoidal glucagon levels remained unchanged, and euglycemia was maintained by peripheral glucose infusion. TDGP was suppressed ~60% by the last 30 min of the experimental period. In contrast, NHGO was suppressed 100% by that time. Coincidentally, hepatic glucose uptake (net hepatic [3H]glucose balance) increased significantly (~4 µmol · kg-1 · min-1). The effects of simultaneous equal increases in peripheral and portal venous insulin were not additive in the suppression of TDGP. However, they were additive in decreasing NHGO as a result of an increase in the uptake of glucose by the liver.

conscious dog; hepatic glucose uptake


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