Fructose augments infection-impaired net hepatic glucose uptake during TPNadministration

During chronic total parenteral nutrition (TPN), net hepatic glucose uptake (NHGU) and net hepatic lactate release (NHLR) are markedly reduced (down a rrow similar to 45 and similar to 65%, respectively) with infection. Becaus e small quantities of fructose are known to augment hepatic glucose uptake and lactate release in normal fasted animals, the aim of this work was to d etermine whether acute fructose infusion with TPN could correct the impairm ents in NHGU and NHLR during infection. Chronically catheterized conscious dogs received TPN for 5 days via the inferior vena cava at a rate designed to match daily basal energy requirements. On the third day of TPN administr ation, a sterile (SHAM, n = 12) or Escherichia coli-containing (INF, n = 11 ) fibrin clot was implanted in the peritoneal cavity. Forty-two hours later , somatostatin was infused with intraportal replacement of insulin(12 +/- 2 vs. 24 +/- 2 muU/ml, SHAM vs. INF, respectively) and glucagon (24 +/- 4 vs . 92 +/- 5 pg/ml) to match concentrations previously observed in sham and i nfected animals. After a 120-min basal period, animals received either sali ne (Sham+S, n = 6; Inf+S, n = 6) or intraportal fructose (0.7 mg . kg(-1) . min(-1); Sham+F, n. = 6; Inf+F, n = 5) infusion far 180 min. Isoglycemia o f 120 mg/dl was maintained with a variable glucose infusion. Combined trace r and arteriovenous difference techniques were used to assess hepatic gluco se metabolism. Acute fructose infusion with TPN augmented NHGU by 2.9 +/- 0 .4 and 2.5 +/- 0.3 mg . kg(-1) . min(-1) in Sham+F and Inf+F, respectively. The majority of liver glucose uptake was stored as glycogen, and NHLR did not increase substantially. Therefore, despite an infection-induced impairm ent in NHGU and different hormonal environments, small amounts of fructose enhanced NHGU similarly in sham and infected animals. Glycogen storage, not lactate release, was the preferential fate of the fructose-induced increas e in hepatic glucose disposal in animals adapted to TPN.