A negative arterial-portal venous glucose gradient decreases skeletal muscle glucose uptake

• Published in: American journal of physiology: endocrinology and metabolism Vol. 275; no. 1; pp. E101 - E111
• Main Authors: Galassetti, Pietro, Shiota, Masakazu, Zinker, Brad A, Wasserman, David H, Cherrington, Alan D
• Format: Journal Article
• Language: English
• Published: United States 01.07.1998
• Subjects: Animals; Blood Glucose - drug effects; Blood Glucose - metabolism; Dogs; Female; Glucagon - administration & dosage; Glucagon - blood; Glucagon - pharmacology; Glucose - metabolism; Hepatic Artery - physiology; Hindlimb; Hyperglycemia - metabolism; Iliac Artery - physiology; Iliac Vein - physiology; Infusions, Intravenous; Insulin - administration & dosage; Insulin - blood; Insulin - pharmacology; Liver - metabolism; Liver Circulation - physiology; Male; Muscle, Skeletal - blood supply; Muscle, Skeletal - drug effects; Muscle, Skeletal - physiology; Portal System - physiology; Portal Vein - physiology; Regional Blood Flow; Somatostatin - administration & dosage; Somatostatin - blood; Somatostatin - pharmacology
• ISSN: 0193-1849; 0002-9513; 1522-1555
• DOI: 10.1152/ajpendo.1998.275.1.E101

Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, Tennessee 37232-0615 The effect of a negative arterial-portal venous (a-pv) glucose gradient on skeletal muscle and whole body nonhepatic glucose uptake was studied in 12 42-h-fasted conscious dogs. Each study consisted of a 110-min equilibration period, a 30-min baseline period, and two 120-min hyperglycemic (2-fold basal) periods (either peripheral or intraportal glucose infusion). Somatostatin was infused along with insulin (3 × basal) and glucagon (basal). Catheters were inserted 17 days before studies in the external iliac artery and hepatic, portal and common iliac veins. Blood flow was measured in liver and hindlimb using Doppler flow probes. The arterial blood glucose, arterial plasma insulin, arterial plasma glucagon, and hindlimb glucose loads were similar during peripheral and intraportal glucose infusions. The a-pv glucose gradient (in mg/dl) was 5 ± 1 during peripheral and 18 ± 3 during intraportal glucose infusion. The net hindlimb glucose uptakes (in mg/min) were 5.0 ± 1.2, 20.4 ± 4.5, and 14.8 ± 3.2 during baseline, peripheral, and intraportal glucose infusion periods, respectively ( P  < 0.01, peripheral vs. intraportal); the hindlimb glucose fractional extractions (in %) were 2.8 ± 0.4, 4.7 ± 0.8, and 3.9 ± 0.5 during baseline, peripheral, and intraportal glucose infusions, respectively ( P < 0.05, peripheral vs. intraportal). The net whole body nonhepatic glucose uptakes (in mg · kg 1 · min 1 ) were 1.6 ± 0.1, 7.9 ± 1.3, and 5.4 ± 1.1 during baseline, peripheral, and intraportal glucose infusion, respectively ( P  < 0.05, peripheral vs. intraportal). In the liver, net glucose uptake was 70% greater during intraportal than during peripheral glucose infusion (5.8 ± 0.7 vs. 3.4 ± 0.4 mg · kg 1 · min 1 ). In conclusion, despite comparable glucose loads and insulin levels, hindlimb and whole body net nonhepatic glucose uptake decreased significantly during portal venous glucose infusion, suggesting that a negative a-pv glucose gradient leads to an inhibitory signal in nonhepatic tissues, among which skeletal muscle appears to be the most important. hyperglycemia; arterial-portal venous glucose gradient