title: Inclusion of low amounts of fructose with an intraportal glucose load increases net hepatic glucose uptake in the presence of relative insulin deficiency in dog.
abstract: The effect of small amounts of fructose on net hepatic glucose uptake (NHGU) during hyperglycemia was examined in the presence of insulinopenia in conscious 42-h fasted dogs. During the study, somatostatin (0.8 microg.kg(-1).min(-1)) was given along with basal insulin (1.8 pmol.kg(-1).min(-1)) and glucagon (0.5 ng.kg(-1).min(-1)). After a control period, glucose (36.1 micromol.kg(-1).min(-1)) was continuously given intraportally for 4 h with (2.2 micromol.kg(-1).min(-1)) or without fructose. In the fructose group, the sinusoidal blood fructose level (nmol/ml) rose from <16 to 176 +/- 11. The infusion of glucose alone (the control group) elevated arterial blood glucose (micromol/ml) from 4.3 +/- 0.3 to 11.2 +/- 0.6 during the first 2 h after which it remained at 11.6 +/- 0.8. In the presence of fructose, glucose infusion elevated arterial blood glucose (micromol/ml) from 4.3 +/- 0.2 to 7.4 +/- 0.6 during the first 1 h after which it decreased to 6.1 +/- 0.4 by 180 min. With glucose infusion, net hepatic glucose balance (micromol.kg(-1).min(-1)) switched from output (8.9 +/- 1.7 and 13.3 +/- 2.8) to uptake (12.2 +/- 4.4 and 29.4 +/- 6.7) in the control and fructose groups, respectively. Average NHGU (micromol.kg(-1).min(-1)) and fractional glucose extraction (%) during last 3 h of the test period were higher in the fructose group (30.6 +/- 3.3 and 14.5 +/- 1.4) than in the control group (15.0 +/- 4.4 and 5.9 +/- 1.8). Glucose 6-phosphate and glycogen content (micromol glucose/g) in the liver and glucose incorporation into hepatic glycogen (micromol glucose/g) were higher in the fructose (218 +/- 2, 283 +/- 25, and 109 +/- 26, respectively) than in the control group (80 +/- 8, 220 +/- 31, and 41 +/- 5, respectively). In conclusion, small amounts of fructose can markedly reduce hyperglycemia during intraportal glucose infusion by increasing NHGU even when insulin secretion is compromised.
authors.affiliation: Dept. of Molecular Physiology and Biophysics, Vanderbilt Univ. School of Medicine, 702 Light Hall, Nashville, TN 37232-0615, USA. masakazu.shiota@vanderbilt.edu
authors.forename: Masakazu
authors.initials: M
authors.lastname: Shiota
authors.forename: Pietro
authors.initials: P
authors.lastname: Galassetti
authors.forename: Kayano
authors.initials: K
authors.lastname: Igawa
authors.forename: Doss W
authors.initials: DW
authors.lastname: Neal
authors.forename: Alan D
authors.initials: AD
authors.lastname: Cherrington
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D004285:Dogs / Q000097:blood / Q000378:metabolism*; D005260:Female; D005632:Fructose / Q000008:administration & dosage* / Q000097:blood / Q000378:metabolism; D005934:Glucagon / Q000378:metabolism; D005947:Glucose / Q000008:administration & dosage* / Q000378:metabolism*; D019298:Glucose-6-Phosphate / Q000378:metabolism; D006854:Hydrocortisone; D007328:Insulin / Q000172:deficiency* / Q000378:metabolism; D019344:Lactic Acid / Q000097:blood; D008099:Liver / Q000378:metabolism*; D008297:Male; D019518:Postprandial Period
chemical_list: D001786:Blood Glucose; D007328:Insulin; D005632:Fructose; D019344:Lactic Acid; D019298:Glucose-6-Phosphate; D005934:Glucagon; D005947:Glucose; D006854:Hydrocortisone