Tumor necrosis factor and interleukin-1 beta: suppression of food intake by direct action in the central nervous system.
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.
Plata-Salamán
C R
CR
Department of Physiology, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
Oomura
Y
Y
Kai
Y
Y
D000818:Animals; D002552:Cerebral Ventricles / Q000187:drug effects / Q000502:physiology*; D005247:Feeding Behavior / Q000187:drug effects*; D007276:Injections, Intraventricular; D007375:Interleukin-1 / Q000008:administration & dosage / Q000494:pharmacology*; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D014409:Tumor Necrosis Factor-alpha / Q000008:administration & dosage / Q000494:pharmacology*
D007375:Interleukin-1; D014409:Tumor Necrosis Factor-alpha