Nonhepatic response to portal glucose delivery in conscious dogs

The glycemic and hormonal responses and net hepatic and nonhepatic glucose uptakes were quantified in conscious 42-h-fasted dogs during a 180-min infu sion of glucose at 10 mg.kg(-1).min(-1) via a peripheral (Pe10, n = 5) or t he portal (Po10, n = 6) vein. Arterial plasma insulin concentrations were n ot different during the glucose infusion in Pe10 and Po10 (37 +/- 6 and 43 +/- 12 muU/ml, respectively), and glucagon concentrations declined similarl y 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 h epatic glucose load significantly greater (36 +/- 3 vs. 46 +/- 5 mg.kg(-1). min(-1) in Pe10 vs. Po10, respectively, P< 0.05). Net hepatic glucose uptak e (NHGU; 1.1 +/- 0.4 vs. 3.1 +/- 0.4 mg.kg(-1).min(-1)) and fractional extr action (0.03 +/- 0.01 vs. 0.07 +/- 0.01) were smaller (P< 0.05) in Pe10 tha n 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.kg(-1 ).min(-1), P< 0.05). Approximately one-half of the difference in NHGU betwe en 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 tissue s, stimulating NHGU and reducing peripheral glucose uptake.