AENDO October 40/4

Hsieh, Po-Shiuan, Mary Courtney Moore, Bess Marshall, Michael J. Pagliassotti, Brian Shay, Dennis Szurkus, Doss W. Neal, and Alan D. Cherrington. The head arterial glucose level is not the reference site for generation of the portal signal in conscious dogs. Am. J. Physiol. 277 (Endocrinol. Metab. 40): E678–E684, 1999.— 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 · kg21 · min21; 3.5-fold increase) and glucagon (0.6 ng·kg21 ·min21; basal) intraportally. Glucose was infused intraportally (22.2 μmol ·kg21 ·min21) 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 6 0.8 μmol ·kg21 ·min21); 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 (20.52 6 0.07 vs. 20.49 6 0.03 mM) and the hepatic glucose loads (339 6 14 vs. 334 6 20 μmol ·kg21 ·min21) were similar in HEADG and HEADS. NHGU was 24.1 6 3.8 and 25.1 6 4.6 μmol ·kg21 ·min21, and nonhepatic glucose uptake was 46.1 6 4.2 and 48.8 6 7.0 μmol ·kg21 ·min21 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.