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Failure of glucagon to induce hepatic phosphoenolpyruvate carboxykinase in endotoxic shock

R D Stith1, R E McCallum

  • 1Department of Physiology, University of Oklahoma Health Sciences Center, Oklahoma City 73190.

Circulatory Shock
|November 1, 1988
PubMed

Insights

Endotoxemia inhibits glucagon

Area of Science:

  • Biochemistry
  • Endocrinology
  • Molecular Biology

Background:

  • Glucocorticoids and glucagon cooperatively regulate phosphoenolpyruvate carboxykinase (PEPCK) mRNA expression.
  • Endotoxemia is known to diminish PEPCK activity, partly due to inhibited glucocorticoid action.
  • The effect of endotoxin on glucagon's induction of PEPCK remains unclear.

Purpose of the Study:

  • To investigate whether endotoxin inhibits glucagon's action to induce hepatic PEPCK activity.

Main Methods:

  • Mice were fasted and treated with endotoxin or saline.
  • Animals received glucose and ad libitum access to food and water.
  • Intravenous glucagon was administered, followed by analysis of plasma glucose and liver PEPCK activity.

Main Results:

  • In control mice, glucagon increased plasma glucose and hepatic PEPCK activity.
  • In endotoxin-treated mice, glucagon failed to increase plasma glucose or PEPCK activity.
  • Endotoxin significantly inhibited glucagon's ability to raise plasma glucose and PEPCK levels.

Conclusions:

  • Glucagon's action to stimulate PEPCK activity and plasma glucose is inhibited during endotoxemia.
  • This finding highlights a mechanism by which endotoxemia disrupts glucose homeostasis.

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