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

M. H. Porter, B. J. Hrupka, W. Langhans, G. J. Schwartz

Research output: Contribution to journalArticle

58 Scopus citations

Abstract

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-1β (IL-1β), 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-1β, 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-1β, LPS, or MDP in the rat and suggest that peripheral administration of immunomodulators produces anorexia via a humoral pathway.

Original languageEnglish (US)
Pages (from-to)R384-R389
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume275
Issue number2 44-2
StatePublished - Sep 2 1998
Externally publishedYes

Keywords

  • Bacterial products
  • Brain- gut communication
  • Cytokine
  • Food intake
  • Interleukin-1β
  • Lipopolysaccharide
  • Muramyl dipeptide

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

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