IL-1 receptor antagonist attenuates sepsis-induced alterations in the IGF system and protein synthesis

Charles H. Lang, Jie Fan, Robert Cooney, Thomas C. Vary

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140 Scopus citations

Abstract

The purpose of the present investigation was to determine whether endogenously produced interleukin (IL)-1 mediates the changes in insulin- like growth factor (IGF) I and IGF binding proteins (IGFBP) induced by chronic abdominal sepsis in rats and to correlate the changes in the IGF system with the alterations in protein synthesis. A constant infusion of IL- 1 receptor antagonist (IL-1ra) was begun after the induction of sepsis and was continued for 5 days. Sepsis decreased IGF-I levels in the blood, liver, and gastrocnemius muscle, increased the content in the kidney, and did not alter IGF-I levels in heart, jejunum, and spleen. IL-1ra attenuated the sepsis-induced decrease in plasma IGF-I and completely prevented the changes in IGF-I observed in liver, kidney, and the gastrocnemius. IGFBP-1 was increased in the blood, liver, and muscle of septic rats. IL-1ra prevented this increase in IGFBP-1 in blood and liver but not in muscle. The rate of in vive protein synthesis was decreased in the gastrocnemius and kidney and unaltered in the heart, liver, jejunum, and spleen. A strong linear correlation existed between levels of IGF-I and the rate of protein synthesis determined simultaneously in the gastrocnemius. These results provide evidence for the role of IL-1 as an endogenous mediator of the sepsis- induced changes in IGF-I and IGFBP-1 and suggest that the accompanying changes in muscle protein synthesis are partially mediated via changes in IGF-I.

Original languageEnglish (US)
Pages (from-to)E430-E437
JournalAmerican Journal of Physiology - Endocrinology and Metabolism
Volume270
Issue number3 33-3
DOIs
StatePublished - 1996

All Science Journal Classification (ASJC) codes

  • Endocrinology, Diabetes and Metabolism
  • Physiology
  • Physiology (medical)

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