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The decrease in hepatic IGF-I gene expression in arthritic rats is not associated with modifications in hepatic GH

A Lopez-Calderon1, I Ibáñez de Caceres, L Soto

  • 1Department of Physiology, Faculty of Medicine, Complutense University, 28040 Madrid, Spain. ALC@eucmax.sim.ucm.es

European Journal of Endocrinology
|May 2, 2001
PubMed
Summary

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Chronic arthritis in rats decreases insulin-like growth factor-I (IGF-I) synthesis. This study found that impaired IGF-I secretion is not due to growth hormone (GH) resistance in the liver.

Area of Science:

  • Endocrinology
  • Inflammation Research

Background:

  • Adjuvant-induced arthritis causes a catabolic state and reduced circulating insulin-like growth factor-I (IGF-I).
  • Acute inflammation is associated with hypermetabolism and growth hormone (GH) insensitivity.

Purpose of the Study:

  • To investigate whether impaired IGF-I secretion in arthritic rats is caused by hepatic GH resistance.
  • To analyze the effect of GH administration on hepatic IGF-I synthesis in arthritic rats.

Main Methods:

  • Male Wistar rats were induced with adjuvant-induced arthritis.
  • Arthritic and control rats received daily injections of recombinant human GH (rhGH) or saline for 8 days.
  • Hepatic GH receptor (GHR) gene expression and IGF-I synthesis were examined.

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Main Results:

  • Arthritic rats showed decreased hepatic IGF-I concentrations and gene expression, but GHR mRNA levels were unchanged.
  • rhGH administration increased body weight gain and hepatic IGF-I synthesis in arthritic rats.
  • Lipopolysaccharide (LPS) administration decreased hepatic IGF-I and IGF-I mRNA, and also reduced GHR mRNA expression.

Conclusions:

  • The reduction in IGF-I synthesis during chronic arthritis is not a consequence of hepatic GH resistance.
  • These findings differentiate the effects of chronic arthritis from acute endotoxemia on GH signaling.