The head arterial glucose level is not the reference site for generation of the portal signal in conscious dogs

The head arterial glucose level is not the reference site for generation of the portal signal in conscious dogs. 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 glucos e level in bringing about the stimulatory effect of portal glucose delivery on net hepatic glucose uptake (NHGU). Each experiment consisted of an 80-m in 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) . min(-1); 3.5-fold increase) and glucagon (0.6 ng kg(-1) . min(-1); basal) intraportally. Glucose was infused intraportally (22.2 mu mol . kg(-1) . m in(-1)) and peripherally as needed to double the hepatic glucose load. In o ne test period, glucose was infused into both vertebral and carotid arterie s (HEAD(G); 22.2 +/- 0.8 mol . kg(-1) . min(-1)); in the other test period, saline was infused into the head arteries (HEAD(s)). One-half of the dogs received HEADG first. When all dogs are considered, the blood arterial-port al glucose gradients (-0.52 +/- 0.07 vs. -0.49 +/- 0.03 mM) and the hepatic glucose loads (339 +/- 14 vs. 334 +/- 20 mu mol kg(-1) min(-1)) were simil ar in HEADG and HEADs. NHGU was 24.1 +/- 3.8 and 25.1 +/- 4.6 mu mol kg(-1) . min(-1), and nonhepatic glucose uptake was 46.1 +/- 4.2 and 48.8 +/- 7.0 mu mol kg(-1) . min(-1) in HEADG and HEADs, respectively. The head arteria l glucose level is not the reference standard used for comparison with the portal glucose level in the generation of the portal signal.