Impact of infection on hepatic disposal of a peripheral glucose
infusion in the conscious dog.
McGuinness, Owen P., Julie Jacobs, Chris Moran, Brooks Lacy.
DEPARTMENT OF MOLECULAR PHYSIOLOGY AND BIOPHYSICS, VANDERBILT
UNIVERSITY, NASHVILLE, TN 37232-0615
APStracts 2:0042E, 1995.
The effect of infection on hepatic uptake and disposal of a continuous
(180 min) intravenous glucose infusion (8 mg/kg/min) was examined in
conscious, 54 hr fasted, chronically catheterized dogs. 36 hours
prior to a study, infection was induced by implantation of a sterile
(SH; n=6), or an E.coli-containing (INF; 2x109 organisms/kg body
weight; n=6), fibrinogen clot into the peritoneal cavity. Hepatic
glucose metabolism was assessed using tracer (3-3H glucose and U-14C
glucose) and arterio-venous difference techniques. Infection
increased the basal rate of glucose appearance (45%); glucose levels
were not altered. In response to glucose infusion the average blood
glucose levels increased to similar levels (140+/-9 vs 147+/-11 mg/dl
in INF and SH), while the 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/min in INF and SH;
p<0.05). The liver remained a persistent lactate consumer (4.1+/
-1.8 [mu]mol/kg/min), whereas the sham group switched to a net
producer of lactate (-3.8+/-1.3 [mu]mol/kg/min). 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.
Received 7 October 1994; accepted in final form 27 February 1995.
APS Manuscript Number E428-4.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 10 March 1995.