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Intracellular glutamine concentration does not decrease in all muscles during sepsis

J H James1, P O Hasselgren, J K King

  • 1Department of Surgery, University of Cincinnati College of Medicine, Ohio 45267-0558.

The Journal of Surgical Research
|June 1, 1993
PubMed
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Sepsis significantly depletes muscle glutamine in the extensor digitorum longus (EDL) but not soleus muscles of rats. This suggests altered glutamine transport contributes to muscle protein breakdown during critical illness.

Area of Science:

  • Biochemistry
  • Physiology
  • Molecular Biology

Background:

  • Sepsis is a critical illness associated with increased muscle protein breakdown, particularly in fast-twitch muscles like the extensor digitorum longus (EDL).
  • Previous research indicates that muscle glutamine levels are reduced in sepsis, but the underlying mechanisms and muscle-specific effects require further elucidation.

Purpose of the Study:

  • To investigate the changes in muscle and plasma amino acid concentrations, focusing on glutamine, in rat soleus and EDL muscles following sepsis induction.
  • To explore the relationship between altered amino acid profiles and hypothesized changes in glutamine transport systems in sepsis.

Main Methods:

  • Rats underwent cecal ligation and puncture to induce sepsis or a sham operation.
  • Plasma and intracellular fluid concentrations of glutamine and other amino acids in soleus and EDL muscles were measured at 4, 8, and 16 hours post-procedure.

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  • Amino acid data were analyzed for correlations to infer alterations in glutamine transport mechanisms.

    • Main Results:

    • Muscle glutamine concentration was significantly reduced (by over 50%) in the EDL muscle of septic rats compared to controls.
    • No significant decrease in glutamine concentration was observed in the soleus muscle of septic rats.
    • Changes in muscle glutamine were not explained by alterations in glutamic acid levels.
    • Correlations between muscle glutamine and other amino acids, such as histidine, suggested a sepsis-induced change in the sarcolemmal glutamine transporter (system Nm).

    Conclusions:

    • Muscle glutamine depletion in EDL, but not soleus, is a key feature of this sepsis model.
    • The findings support the hypothesis that altered glutamine transport contributes to the dysregulation of muscle protein metabolism during catabolic states like sepsis.
    • This study strengthens the link between muscle glutamine levels and muscle protein breakdown under septic conditions.