AJP - Endocrinology and Metabolism, Vol 269, Issue 5 E852-E857, Copyright © 1995 by American Physiological Society
Interleukin-1 beta-induced anorexia and pyrexia in rat: relationship to hypothalamic neuropeptide Y
H. D. McCarthy, S. Dryden and G. Williams
Department of Medicine, University of Liverpool, United Kingdom.
We investigated the effect of recombinant human interleukin-1 beta (rhIL-1
beta)-induced anorexia and pyrexia on the hypothalamic neuropeptide Y
(NPY)-ergic system, which stimulates feeding and reduces thermogenesis. In
meal-fed rats, food intake decreased by 83%, 90 min after IL-1 beta
treatment (1.3 micrograms/100 g ip; n - 8) vs. controls. NPY concentrations
were significantly higher in the medial preoptic area (MPO),
paraventricular (PVN), ventromedial (VMN), and dorsomedial (DMN) nuclei but
unchanged in the arcuate nucleus (ARC) in both IL-1 beta-treated and
pair-fed groups. Indomethacin (0.25 mg/100 g ip) reduced IL-1 beta-induced
anorexia and tended to normalize NPY concentrations. In study 2, IL-1 beta
increased core temperature by 1.1 degrees C above preinjection values (P
< 0.001) and significantly raised NPY concentrations in the MPO, PVN,
VMN, and DMN compared with controls, 60 min postinjection. Indomethacin
prevented the pyrexia and normalized hypothalamic NPY levels. As NPY
concentrations were not increased in the ARC (the hypothalamic site of
synthesis), we suggest that the increased NPY levels may result from
blocked release, which would be in accord with the known experimental
effects of NPY.
