The interaction of equal increments in arterial and portal vein
insulin on hepatic glucose production in the dog.
Sindelar, Dana K., Chang A. Chu, Doss W. Neal, and Alan D.
Cherrington.
Department of Molecular Physiology and Biophysics, Vanderbilt
University School of Medicine, Nashville, TN 37232-0615
APStracts 4:0176E, 1997.
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 A-V 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 experimental period. In
contrast, NHGO was suppressed 100% by that time. Coincidentally,
hepatic glucose uptake (net hepatic 3H-glucose balance) increased
significantly (4 [mu]mol.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.
Received 4 April 1997; accepted in final form 5 August 1997.
APS Manuscript Number E154-7.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1997 The American Physiological Society.
Published in APStracts on 27 August 1997