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1 Department of Molecular Physiology & Biophysics and Diabetes Research & Training Center, Vanderbilt University School of Medicine, Nashville, TN, USA
2 Department of Molecular Physiology & Biophysics and Diabetes Research & Training Center, Vanderbilt University School of Medicine, Nashville, TN, USA; Wellstat Therapeutics, Gaithersburg, MD, USA
* To whom correspondence should be addressed. E-mail: genie.moore{at}vanderbilt.edu.
Portal infusion of glucose in the mouse at a rate equivalent to basal endogenous glucose production causes hypoglycemia, while peripheral infusion at the same rate
causes significant hyperglycemia. We used tracer and arteriovenous difference techniques in conscious 42-h-fasted dogs to determine their response to the same treatments. The studies consisted of 3 periods: equilibration (100 min), basal (40 min), and experimental
(180 min), during which glucose was infused at 13.7 µmol.kg-1.min-1 into a peripheral (PE, n=5) or the hepatic portal (PO, n=5) vein. Arterial blood glucose increased ~0.8
mmol/l in both groups. Arterial and hepatic sinusoidal insulin concentrations were not significantly different between groups. PE exhibited an increase in nonhepatic glucose uptake (non-HGU; 
8.6±1.2 µmol.kg-1.min-1) within 30 min, whereas PO showed a slight suppression (-3.7±3.1 µmol.kg-1.min-1). PO shifted from net hepatic glucose output
(NHGO) to uptake (NHGU; 2.5±2.8 µmol.kg-1.min-1) within 30 min, but PE still exhibited NHGO (6.0±1.9 µmol.kg-1.min-1) at that time and did not initiate NHGU until after 90 min. Glucose Ra and Rd did not differ between groups. The response to the two infusion routes was markedly different. Peripheral infusion caused a rapid enhancement of non-HGU, while portal delivery quickly activated NHGU. As a result, both groups maintained near-euglycemia. The dog glucoregulates more rigorously than the mouse in response to both portal and peripheral glucose delivery.
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