Tumor necrosis factor and interleukin-1 beta: suppression of food intake by direct action in the central nervous system

Brain Res. 1988 May 10;448(1):106-14. doi: 10.1016/0006-8993(88)91106-7.


Intracerebroventricular microinfusion of recombinant human tumor necrosis factor (rhTNF) and recombinant human interleukin-1 beta (rhIL-1 beta) suppressed food intake in rats. Central infusion of heat-inactivated rhTNF and rhIL-1 beta, bovine serum albumin, heparin or transforming growth factor-beta had no such effect. Central infusion of rhIL-1 beta did not affect the dipsogenic response to central administration of angiotensin II. Peripheral administration of rhTNF and rhIL-1 beta in doses equivalent to or higher than those administered centrally had no effect. Electrophoretically applied rhTNF and rhIL-1 beta specifically suppressed the activity of glucose-sensitive neurons in the lateral hypothalamic area. Glucose-insensitive neurons were little affected. The results suggest that TNF and IL-1 beta act directly in the central nervous system to suppress feeding, and this effect may be operative during acute and chronic disease.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cerebral Ventricles / drug effects
  • Cerebral Ventricles / physiology*
  • Feeding Behavior / drug effects*
  • Injections, Intraventricular
  • Interleukin-1 / administration & dosage
  • Interleukin-1 / pharmacology*
  • Male
  • Rats
  • Rats, Inbred Strains
  • Tumor Necrosis Factor-alpha / administration & dosage
  • Tumor Necrosis Factor-alpha / pharmacology*


  • Interleukin-1
  • Tumor Necrosis Factor-alpha