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Department of Molecular Physiology and Biophysics and Diabetes Research and Training Center, Vanderbilt University, Nashville, Tennessee 37232-0615
The aim of this study was to assess the decay of
the effect of the portal signal on net hepatic glucose uptake (NHGU).
Experiments were performed on five 42-h-fasted conscious dogs. After
the 40-min basal period, somatostatin was given peripherally along with
insulin (1.8 pmol · kg
1 · min
1)
and glucagon (0.65 ng · kg
1 · min
1)
intraportally. In the first experimental period (Pe-GLU-1; 90 min),
glucose was infused into a peripheral vein to double the glucose load
to the liver (HGL). In the second experimental period (Po-GLU; 90 min),
glucose (20.1 µmol · kg
1 · min
1)
was infused intraportally and the peripheral glucose infusion was
reduced to maintain the same HGL. In the third period (Pe-GLU-2; 120 min), the portal glucose infusion was stopped and the peripheral glucose infusion was increased to again sustain HGL. Arterial insulin
levels (42 ± 3, 47 ± 3, 43 ± 3 pmol/l) were basal and similar in the Pe-GLU-1, Po-GLU, and Pe-GLU-2 periods, respectively. Arterial glucagon levels were also basal and similar (51 ± 3, 49 ± 2, 46 ± 2 ng/l) in the three experimental periods. The
glucose loads to the liver were 251 ± 11, 274 ± 14, and 276 ± 12 µmol · kg
1 · min
1,
respectively. NHGU was 6.3 ± 2.4, 19.1 ± 2.8, and 9.2 ± 1.2 µmol · kg
1 · min
1,
and nonhepatic glucose uptake (non-HGU) was 23.6 ± 3.0, 5.3 ± 1.8, and 25.5 ± 3.7 µmol · kg
1 · min
1
in the three periods, respectively. Cessation of the portal signal for
only 10 min shifted NHGU and non-HGU to 9.4 ± 2.2 and 25.0 ± 2.8 µmol · kg
1 · min
1,
respectively; thus the effect of the portal signal was rapidly reversed
both at the liver and peripheral tissues.
glucose; liver; liver nerve
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