Hepatic glucose uptake rapidly decreases after removal of the portal signal in conscious dogs

The aim of this study was to assess the decay of the effect of the portal s ignal on net hepatic glucose uptake (NHGU). Experiments were performed on f ive 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 gl ucagon (0.65 ng.kg(-1).min(-1)) intraportally. In the first experimental pe riod (Pe-GLU-1; 90 min), glucose was infused into a peripheral vein to doub le the glucose load to the Liver (HGL). In the second experimental period ( Po-GLU; 90 min), glucose (20.1 mu mol.kg(-1).min(-1)) was infused intraport ally and the peripheral glucose infusion was reduced to maintain the same H GL. In the third period (Pe-GLU-2; 120 min), the portal glucose infusion wa s stopped and the peripheral glucose infusion was increased to again sustai n HGL. Arterial insulin levels (42 +/- 3, 47 +/- 3, 43 +/- 3 pmol/l) were b asal and similar in the Pe-GLU-1, Po-GLU, and Pe-GLU-2 periods, respectivel y. 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 th e liver were 251 +/- 11, 274 +/- 14, and 276 +/- 12 mu mol.kg(-1).min(-1), respectively. NHGU was 6.3 +/- 2.4, 19.1 +/- 2.8, and 9.2 +/- 1.2 mu mol.kg (-1).min(-1), and nonhepatic glucose uptake (non-HGU) was 23.6 +/- 3.0, 5.3 +/- 1.8, and 25.5 +/- 3.7 mu mol.kg(-1).min(-1) in the three periods, resp ectively. Cessation of the portal signal for only 10 min shifted NHGU and n on-HGU to 9.4 +/- 2.2 and 25.0 +/- 2.8 mu mol.kg(-1).min(-1), respectively; thus the effect of the portal signal was rapidly reversed both at the live r and peripheral tissues.