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Department of Molecular Physiology and Biophysics, and Diabetes Research and Training Center, Vanderbilt University, Nashville, Tennessee 37232-0615
Experiments were performed on twelve
42-h-fasted, conscious dogs to determine whether the head arterial
glucose level is used as a reference standard for comparison with the
portal glucose level in bringing about the stimulatory effect of portal
glucose delivery on net hepatic glucose uptake (NHGU). Each experiment consisted of an 80-min equilibration, a 40-min control, and two 90-min
test periods. After the control period, somatostatin was given along
with insulin (7.2 pmol · kg
1 · min1;
3.5-fold increase) and glucagon (0.6 ng · kg1 · min1;
basal) intraportally. Glucose was infused intraportally (22.2 µmol · kg1 · min1)
and peripherally as needed to double the hepatic glucose load. In one
test period, glucose was infused into both vertebral and carotid
arteries (HEADG; 22.2 ± 0.8 µmol · kg1 · min1);
in the other test period, saline was infused into the head arteries
(HEADS). One-half of the dogs
received HEADG first. When all
dogs are considered, the blood arterial-portal glucose gradients (
0.52 ± 0.07 vs. 0.49 ± 0.03 mM) and
the hepatic glucose loads (339 ± 14 vs. 334 ± 20 µmol · kg1 · min1)
were similar in HEADG and
HEADS. NHGU was 24.1 ± 3.8 and
25.1 ± 4.6 µmol · kg1 · min1,
and nonhepatic glucose uptake was 46.1 ± 4.2 and 48.8 ± 7.0 µmol · kg1 · min1
in HEADG and
HEADS, respectively. The head
arterial glucose level is not the reference standard used for
comparison with the portal glucose level in the generation of the
portal signal.
liver; brain; liver nerve
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