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1 Department of Molecular Physiology and Biophysics and 2 Diabetes Research and Training Center, Vanderbilt University School of Medicine, Nashville, Tennessee 37232-0615
The glycemic and hormonal responses and net hepatic and
nonhepatic glucose uptakes were quantified in conscious 42-h-fasted dogs during a 180-min infusion of glucose at 10 mg · kg
1 · min1 via a
peripheral (Pe10, n = 5) or the portal (Po10,
n = 6) vein. Arterial plasma insulin concentrations
were not different during the glucose infusion in Pe10 and Po10
(37 ± 6 and 43 ± 12 µU/ml, respectively), and glucagon
concentrations declined similarly throughout the two studies. Arterial
blood glucose concentrations during glucose infusion were not different
between groups (125 ± 13 and 120 ± 6 mg/dl in Pe10 and
Po10, respectively). Portal glucose delivery made the hepatic glucose
load significantly greater (36 ± 3 vs. 46 ± 5 mg · kg1 · min1 in Pe10 vs.
Po10, respectively, P < 0.05). Net hepatic glucose uptake (NHGU; 1.1 ± 0.4 vs. 3.1 ± 0.4 mg · kg1 · min1) and
fractional extraction (0.03 ± 0.01 vs. 0.07 ± 0.01) were smaller (P < 0.05) in Pe10 than in Po10. Nonhepatic
(primarily muscle) glucose uptake was correspondingly increased in Pe10
compared with Po10 (8.9 ± 0.4 vs. 6.9 ± 0.4 mg · kg1 · min1,
P < 0.05). Approximately one-half of the difference in
NHGU between groups could be accounted for by the difference in hepatic glucose load, with the remainder attributable to the effect of the
portal signal itself. Even in the absence of somatostatin and fixed
hormone concentrations, the portal signal acts to alter partitioning of
a glucose load among the tissues, stimulating NHGU and reducing
peripheral glucose uptake.
portal vein; liver; insulin sensitivity; glucose load
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