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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 · min1).
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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