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Role of prostaglandins in tumour necrosis factor induced weight loss

S M Mahony1, M J Tisdale

  • 1CRC Experimental Chemotherapy Group, Aston University, Birmingham, UK.

British Journal of Cancer
|July 1, 1989
PubMed

Insights

Tumor necrosis factor alpha (TNF-alpha) causes weight loss by reducing food intake, potentially through prostaglandin E2 (PGE2). However, inhibiting PGE2 did not prevent TNF-alpha-induced weight loss, suggesting prostaglandins are not involved.

Area of Science:

  • Immunology
  • Physiology
  • Pharmacology

Background:

  • Tumor necrosis factor alpha (TNF-alpha) is a pro-inflammatory cytokine implicated in various physiological processes.
  • Prostaglandin E2 (PGE2) is a lipid mediator involved in inflammation and appetite regulation.

Purpose of the Study:

  • To investigate the role of prostaglandin E2 (PGE2) in mediating the anorectic and body weight-reducing effects of tumor necrosis factor alpha (TNF-alpha).

Main Methods:

  • Administration of TNF-alpha or PGE2 to female NMRI mice.
  • Measurement of body weight, food intake, water intake, and carcass water content.
  • Assessment of PGE2 production by spleen cells.
  • Inhibition of PGE2 production using indomethacin.

Main Results:

  • Both TNF-alpha and PGE2 administration led to decreased body weight, food intake, water intake, and carcass water content.
  • TNF-alpha treatment enhanced PGE2 production by spleen cells.
  • Indomethacin administration partially inhibited TNF-alpha-induced weight loss and completely inhibited PGE2 production when given 2 hours prior to TNF-alpha.
  • Indomethacin did not significantly affect TNF-alpha-induced weight loss when administered 0.5-1.5 hours before TNF-alpha, despite inhibiting PGE2 production.

Conclusions:

  • While TNF-alpha administration stimulates PGE2 production, prostaglandins do not appear to mediate the anorectic or body weight-reducing effects of TNF-alpha.
  • The mechanism by which TNF-alpha causes anorexia and weight loss may not involve PGE2.

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