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Am J Physiol Regul Integr Comp Physiol 275: R384-R389, 1998;
0363-6119/98 $5.00
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Vol. 275, Issue 2, R384-R389, August 1998

Vagal and splanchnic afferents are not necessary for the anorexia produced by peripheral IL-1beta , LPS, and MDP

M. H. Porter1, B. J. Hrupka1, W. Langhans1, and G. J. Schwartz2

1 Institute for Animal Sciences, Physiology and Animal Husbandry, Swiss Federal Institute of Technology, 8092 Zurich, Switzerland; and 2 Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205

We investigated the extrinsic gut neural mediation of the suppression of food intake in male Sprague-Dawley rats induced by peripheral intraperitoneal administration of 2 µg/kg interleukin-1beta (IL-1beta ), 100 µg/kg bacterial lipopolysaccharide (LPS), and 2 mg/kg muramyl dipeptide (MDP). Food intake during the first 3 and 6 h of the dark cycle was measured in rats with subdiaphragmatic vagal deafferentation (n = 9), celiac superior mesenteric ganglionectomy (n = 9), combined vagotomy and ganglionectomy (n = 9), and sham deafferentation (n = 9). IL-1beta , LPS, and MDP suppressed food intake at 3 and 6 h in all surgical groups. The results demonstrate that neither vagal nor nonvagal afferent nerves from the upper gut are necessary for the feeding-suppressive effects of intraperitoneal IL-1beta , LPS, or MDP in the rat and suggest that peripheral administration of immunomodulators produces anorexia via a humoral pathway.

interleukin-1beta ; lipopolysaccharide; muramyl dipeptide; food intake; brain-gut communication; cytokine; bacterial products


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