AJP - Regulatory, Integrative and Comparative Physiology, Vol 258, Issue 4 987-R993, Copyright © 1990 by American Physiological Society
Ethanol attenuates endotoxin-enhanced glucose utilization
P. E. Molina, C. H. Lang, G. J. Bagby and J. J. Spitzer
Department of Physiology, Louisiana State University Medical Center, New Orleans 70112.
Ethanol (EtOH) is known to alter various aspects of cellular metabolism.
Among these, the blunting of the increased rate of glucose production and
utilization by the host after the administration of endotoxin may be an
important factor in the increased susceptibility to infections. Therefore
the present study was conducted to determine which tissues are responsible
for the attenuation of the endotoxin-induced increase in whole body glucose
utilization after acute EtOH administration. In vivo glucose metabolic rate
(Rg) of different organs was investigated in conscious rats by the tracer
2-deoxy-D-glucose technique. Rats received a slow intravenous bolus
injection of EtOH (275 mg/100 g body wt of a 20% wt/vol solution) followed
by a continuous infusion (25 mg/100 g body wt) that was maintained
throughout the experimental period. Thirty minutes after initiation of the
EtOH treatment, Escherichia coli endotoxin (100 micrograms/100 g body wt)
was administered intravenously. Time-matched control animals received an
equal volume of saline. EtOH alone affected Rg only in gastrocnemius muscle
(30% decrease) and adipose tissue (twofold increase). Endotoxin alone
increased Rg in all tissues examined except in heart and brain. Prior
administration of EtOH inhibited the endotoxin-induced increased Rg in
skeletal muscle (regardless of fiber type), ileum, liver, adipose tissue,
and kidney, blunted the increase in spleen and lung, and did not alter the
increased Rg in skin. Brain showed a 20% decrease in Rg in response to EtOH
and endotoxin administration. The EtOH-attenuated increase in glucose
utilization in the macrophage-rich tissues of endotoxin-treated rats may be
a reflection of an impaired capacity of these tissues to respond to
infection.
