HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 292/1/R258    most recent 00511.2006v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (6) Citing Articles via Google Scholar Google Scholar Articles by Elander, L. Articles by Blomqvist, A. Search for Related Content PubMed PubMed Citation Articles by Elander, L. Articles by Blomqvist, A.

APPETITE, OBESITY, DIGESTION, AND METABOLISM

IL-1 and LPS induce anorexia by distinct mechanisms differentially dependent on microsomal prostaglandin E synthase-1

¹Division of Cell Biology, Department of Biomedicine and Surgery, Faculty of Health Sciences, Linköping University, and ²Clinical Pathology and Cytology, Center for Laboratory Medicine, University Hospital, Linköping, Sweden

Submitted 18 July 2006 ; accepted in final form 30 August 2006

Recent work demonstrated that the febrile response to peripheral immune stimulation with proinflammatory cytokine IL-1 or bacterial wall lipopolysaccharide (LPS) is mediated by induced synthesis of prostaglandin E₂ by the terminal enzyme microsomal prostaglandin E synthase-1 (mPGES-1). The present study examined whether a similar mechanism might also mediate the anorexia induced by these inflammatory agents. Transgenic mice with a deletion of the Ptges gene, which encodes mPGES-1, and wild-type controls were injected intraperitoneally with IL-1, LPS, or saline. Mice were free fed, and food intake was continuously monitored with an automated system for 12 h. Body weight was recorded every 24 h for 4 days. The IL-1 induced anorexia in wild-type but not knock-out mice, and so it was almost completely dependent on mPGES-1. In contrast, LPS induced anorexia of the same magnitude in both phenotypes, and hence it was independent of mPGES-1. However, when the mice were prestarved for 22 h, LPS induced anorexia and concomitant body weight loss in the knock-out animals that was attenuated compared with the wild-type controls. These data suggest that IL-1 and LPS induce anorexia by distinct immune-to-brain signaling pathways and that the anorexia induced by LPS is mediated by a mechanism different from the fever induced by LPS. However, nutritional state and/or motivational factors also seem to influence the pathways for immune signaling to the brain. Furthermore, both IL-1 and LPS caused reduced meal size but not meal frequency, suggesting that both agents exerted an anhedonic effect during these experimental conditions.

inflammation; food intake; body weight; cytokine; prostaglandin E₂

This article has been cited by other articles:

				B. Samuelsson, R. Morgenstern, and P.-J. Jakobsson Membrane Prostaglandin E Synthase-1: A Novel Therapeutic Target Pharmacol. Rev., September 1, 2007; 59(3): 207 - 224. [Abstract] [Full Text] [PDF]