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Tumor necrosis factor-alpha inhibits albumin gene expression in a murine model of cachexia.

D A Brenner1, M Buck, S P Feitelberg

  • 1Department of Medicine, University of California, San Diego 92093.

The Journal of Clinical Investigation
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Summary

Tumor necrosis factor-alpha (TNF alpha) selectively suppresses albumin gene expression in a mouse model of cachexia. This inhibition occurs before weight loss, impacting albumin synthesis and serum levels.

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Area of Science:

  • Biochemistry
  • Molecular Biology
  • Pathophysiology

Background:

  • Decreased serum albumin levels are observed in cachexia associated with infection, inflammation, and cancer.
  • Tumor necrosis factor-alpha (TNF alpha) is elevated in cachexia-associated diseases and induces cachexia in animal models.

Purpose of the Study:

  • To investigate the regulation of albumin gene expression by TNF alpha in vivo.
  • To determine if TNF alpha directly impacts albumin synthesis and mRNA levels during cachexia.

Main Methods:

  • Utilized a mouse model of cachexia by inoculating nude mice with Chinese hamster ovary cells expressing human TNF alpha.
  • Assessed serum albumin levels, albumin synthesis, and albumin mRNA levels.
  • Employed in situ hybridization and nuclear transcription assays to evaluate gene expression in the liver.

Main Results:

  • TNF alpha mice exhibited cachexia, decreased serum albumin, reduced albumin synthesis, and lower albumin mRNA levels.
  • Albumin mRNA steady-state levels decreased significantly (~90%) even before observable weight loss.
  • Hepatic nuclei from TNF alpha mice showed reduced activity in transcribing the albumin gene compared to controls.

Conclusions:

  • TNF alpha selectively inhibits albumin gene expression in this cachexia model.
  • The suppression of albumin expression by TNF alpha precedes the onset of significant weight loss.
  • This finding provides insight into the mechanisms underlying hypoalbuminemia in cachectic conditions.