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Related Experiment Videos

[Energy substrate metabolism during stress]

H Sugimoto1

  • 1Department of Traumatology and Critical Care Medicine, Osaka University School of Medicine, Suita, Japan.

Nihon Geka Gakkai Zasshi
|September 1, 1996
PubMed
Summary

Stress causes hyperglycemia and elevated lactate by affecting energy metabolism, potentially benefiting the body by ensuring glucose supply to vital organs like the brain.

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Area of Science:

  • Biochemistry
  • Physiology
  • Endocrinology

Context:

  • Stress response involves increased resting energy expenditure (REE), hyperglycemia, and protein catabolism.
  • Neurohormonal and cytokine mediators drive stress-induced hypermetabolic responses.
  • Hyperglycemia during stress, termed 'stress diabetes', is a complex metabolic alteration.

Purpose:

  • To elucidate the mechanisms behind stress-induced hyperglycemia and hyperlactatemia.
  • To investigate glucose disposal and uptake alterations during critical illness.
  • To understand the role of insulin-regulatable glucose transporter (GLUT4) and postreceptor signaling.

Summary:

  • Stress triggers hyperglycemia and hyperlactatemia, potentially via postreceptor insulin resistance and altered pyruvate dehydrogenase activity.
  • While glucose disposal may seem impaired, overall glucose uptake in non-insulin-dependent tissues can increase during sepsis or TNF infusion.
  • Hyperlactatemia may contribute to gluconeogenesis, and sustained hyperglycemia ensures essential glucose supply to the brain and erythrocytes.

Impact:

  • Understanding these metabolic shifts is crucial for managing critically ill patients.
  • This research clarifies the pathophysiology of 'stress diabetes' and its implications.
  • Recognizing hyperglycemia as a potentially beneficial adaptive response during stress can inform clinical management strategies.

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