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IL-1β and LPS induc...
IL-1β and LPS induce anorexia by distinct mechanisms differentially dependent on microsomal prostaglandin E synthase-1
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- Elander, Louise, 1980- (författare)
- Linköpings universitet,Avdelningen för medicinsk cellbiologi,Hälsouniversitetet
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- Engström, Linda, 1976- (författare)
- Linköpings universitet,Avdelningen för medicinsk cellbiologi,Hälsouniversitetet
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- Hallbeck, Martin, 1970- (författare)
- Östergötlands Läns Landsting,Linköpings universitet,Hälsouniversitetet,Avdelningen för medicinsk cellbiologi,Klinisk patologi och klinisk genetik
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- Blomqvist, Anders, 1949- (författare)
- Linköpings universitet,Avdelningen för medicinsk cellbiologi,Hälsouniversitetet
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(creator_code:org_t)
- American Physiological Society, 2007
- 2007
- Engelska.
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Ingår i: American Journal of Physiology. Regulatory Integrative and Comparative Physiology. - : American Physiological Society. - 0363-6119 .- 1522-1490. ; 292:1, s. R258-R267
- Relaterad länk:
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https://urn.kb.se/re...
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https://doi.org/10.1...
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Abstract
Ämnesord
Stäng
- Recent work demonstrated that the febrile response to peripheral immune stimulation with proinflammatory cytokine IL-1β 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-1β, 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-1β 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 wildtype controls. These data suggest that IL-1β 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-1β and LPS caused reduced meal size but not meal frequency, suggesting that both agents exerted an anhedonic effect during these experimental conditions. Copyright © 2007 the American Physiological Society.
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- MEDICINE
- MEDICIN
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- art (ämneskategori)
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