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Related Experiment Videos

Ethanol attenuates endotoxin-enhanced glucose utilization.

P E Molina1, C H Lang, G J Bagby

  • 1Department of Physiology, Louisiana State University Medical Center, New Orleans 70112.

The American Journal of Physiology
|April 1, 1990
PubMed
Summary

Ethanol (EtOH) administration impairs the body's glucose metabolism response to endotoxin, particularly in key tissues. This suggests a mechanism for increased infection susceptibility when alcohol is consumed during illness.

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Area of Science:

  • Metabolic Physiology
  • Toxicology
  • Immunology

Background:

  • Ethanol (EtOH) alters cellular metabolism, potentially impacting infection susceptibility.
  • Endotoxin administration typically increases host glucose production and utilization.
  • Acute EtOH administration may blunt this endotoxin-induced metabolic response.

Purpose of the Study:

  • To identify specific tissues responsible for the attenuation of endotoxin-induced glucose utilization by acute EtOH.
  • To investigate the impact of EtOH and endotoxin on organ-specific glucose metabolism.

Main Methods:

  • Conscious rats were used to measure in vivo glucose metabolic rate (Rg) using the 2-deoxy-D-glucose tracer technique.
  • Animals received intravenous EtOH followed by Escherichia coli endotoxin.

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  • Organ Rg was assessed in EtOH-treated, endotoxin-treated, and control groups.

    • Main Results:

    • EtOH alone decreased Rg in gastrocnemius muscle and increased it in adipose tissue.
    • Endotoxin alone increased Rg in most tissues, except heart and brain.
    • Prior EtOH administration inhibited endotoxin-induced Rg increases in skeletal muscle, ileum, liver, adipose tissue, and kidney, while blunting it in spleen and lung. Brain Rg decreased.

    Conclusions:

    • Acute EtOH administration significantly attenuates the endotoxin-induced increase in glucose utilization across multiple tissues.
    • The blunted response in macrophage-rich tissues may indicate impaired host defense capacity during infection when EtOH is present.
    • Understanding these EtOH-mediated metabolic changes is crucial for addressing infection susceptibility.