Interleukin-1 (IL-1), IL-6, and tumor necrosis factor (TNF) are thought to mediate the onset of anorexia with infection. Animal studies suggest that gastric stasis accompanies IL-1-induced anorexia, and that food intake and gastric emptying of IL-1-injected rats are improved by pretreatment with ibuprofen (ibu), an inhibitor of prostaglandin (PG) synthesis. The purpose of the present study was to determine if gastric stasis accompanies the reduced food intake induced by intraperitoneal injection of TNFa or IL-6 and whether these effects are mediated by PG. Injection of TNFa reduced food intake of fasted rats, but did not affect gastric emptying; injection of IL-6 reduced both food intake and gastric emptying. Pretreatment with 10 mg/kg ibu improved food intake of TNFa-injected animals, but did not affect food intake or gastric emptying of IL-6-injected animals. These data indicate that although IL-6 and TNFa have overlapping effects on food intake, the mechanisms of action are not identical. Delayed gastric emptying does not play a major role in the anorexigenic effects of TNFa, and PG synthesis does not play a major role in the anorexigenic effects of IL-6. These findings may be helpful in the development of interventions to improve nutritional intake during infection.
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