NEUROPEPTIDE-Y BLOCKS AND REVERSES INTERLEUKIN-1-BETA-INDUCED ANOREXIA IN RATS

Neuropeptide Y (NPY) increases feeding by direct action in the central nervous system (CNS). Interleukin-1 beta (IL-1 beta), on the other ha nd, induces anorexia when administered ICV at estimated pathophysiolog ical (e.g., yielded by 1.0 ng/rat dose) and pharmacological (greater t han or equal to 4.0 ng) concentrations in the cerebrospinal fluid (CSF ). In the present study, we investigated NPY/IL-1 beta interactions us ing the ICV administration. ICV microinfusion of NPY (5.0 mu g) signif icantly increased 2-h food intake (by 89%), whereas IL-1 beta decrease d 2-h food intake (32% decrease with 1.0 ng/rat; 53% with 4.0 ng/rat; and 51% with 8.0 ng/rat). NPY (5.0 pg) blocked the anorexic effect ind uced by all doses of IL-1 beta when both compounds were administered c oncomitantly. Central infusion of NPY was also able to induce feeding in IL-1 beta-pretreated rats exhibiting marked anorexia. The results s how that ICV-administered NPY blocks and reverses the anorexia induced by estimated pathophysiological and pharmacological concentrations of IL-1 beta in rats. A second interpretation of a data subset is that I L-1 beta attenuates or blocks NPY-induced increase in feeding dependin g on the IL-1 beta dose used. Blockage and reversal of IL-1 beta-induc ed anorexia by NPY suggest the importance in studying cytokine-peptide interactions in the regulation of feeding behavior. Understanding the se endogenous interactions may produce strategies with potential thera peutic implications for chronic diseases associated with long-term ano rexia.