IMPACT OF INFECTION ON HEPATIC DISPOSAL OF A PERIPHERAL GLUCOSE-INFUSION IN THE CONSCIOUS DOG

The effect of infection on hepatic uptake and disposal of a continuous (180-min) intravenous glucose infusion (8 mg . kg(-1). min(-1)) was examined in conscious, M-h-fasted, chronically catheterized dogs. Thirty-six hours before a study, either infection was induced by implantation of an Escherichia coli-containing (INF; 2 x 10(9) organisms/kg body wt; n = 6) fibrinogen clot, or a sterile (SH; n = 6) clot was implanted into the peritoneal cavity. Hepatic glucose metabolism was assessed using tracer ([3-H-3]glucose and [U-C-14]glucose) and arteriovenous difference techniques. Infection increased the basal rate of glucose appearance (45%); glucose levels were not altered. In response to glucose infusion, average blood glucose levels increased to similar levels (140 +/- 9 vs. 147 +/- 11 mg/dl in INF and SH, respectively), whereas arterial insulin levels were higher in the infected group during the last hour of the glucose infusion (77 +/- 10 vs. 41 +/- 5 mu U/ml in INF vs. SH). Infection impaired net hepatic glucose uptake (0.6 +/- 0.5 and 2.7 +/- 0.7 mg . kg-1 . min-1 in INF and SH; P < 0.05). The liver remained a persistent lactate consumer (4.1 +/- 1.8 mu mol . kg(-1). min(-1)), whereas the sham group became a net producer of lactate (-3.8 +/- 1.3 mol . kg(-1). min(-1)). Infection decreased net hepatic glycogen deposition by 53%. In conclusion, infection impairs net hepatic glucose uptake and glycogen deposition despite an exaggerated increase in insulin levels.