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 (R(g)) 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 μg/100 g body wt) was administered intravenously. Time-matched control animals received an equal volume of saline. EtOH alone affected R(g) only in gastrocnemius muscle (30% decrease) and adipose tissue (twofold increase). Endotoxin alone increased R(g) in all tissues examined except in heart and brain. Prior administration of EtOH inhibited the endotoxin-induced increased R(g) 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 R(g) in skin. Brain showed a 20% decrease in R(g) 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.
|Original language||English (US)|
|Journal||American Journal of Physiology - Regulatory Integrative and Comparative Physiology|
|Issue number||4 27-4|
|State||Published - 1990|
All Science Journal Classification (ASJC) codes
- Physiology (medical)