Interleukin-1[beta]-induced anorexia and pyrexia in the rat:
relationship to hypothalamic neuropeptide y.
McCarthy, H. David, Simon Dryden, and Gareth Williams.
Diabetes and Metabolism Research Group, Department of Medicine,
University of Liverpool, PO Box 147, Liverpool L69 3BX, U.K.
APStracts 2:0131E, 1995.
We investigated the effect of interleukin-1[beta]- (rhIL-1[beta])
induced anorexia and pyrexia on the hypothalamic neuropeptide Yergic
(NPY) system, which stimulates feeding and reduces thermogenesis. In
meal-fed rats, food intake decreased by 83%, 90 minutes after IL
-1[beta] treatment (1.3 _g/100 g i.p; n = 8) versus 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
i.p.) reduced IL-1[beta]-induced anorexia and tended to normalize NPY
concentrations. In study two, IL-1[beta] increased core temperature
by 1.1 oC above pre-injection values (P<0.001) and significantly
raised NPY concentrations in the MPO, PVN, VMN and DMN compared with
controls, 60 minutes post injection. 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.
Received 25 January 1995; accepted in final form 6 June 1995.
APS Manuscript Number E34-5.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 6 July 1995.