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Related Experiment Video

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Assessing Activity-based Anorexia in Mice

Assessing Activity-based Anorexia in Mice

Published on: May 14, 2018

Signals generating anorexia during acute illness.

Wolfgang Langhans¹

¹Physiology and Behaviour Group, Institute of Animal Sciences, ETH Zurich, Schwerzenbach, Switzerland. wolfgang-langhans@ethz.ch

The Proceedings of the Nutrition Society

|July 20, 2007

Summary

Lipopolysaccharides (LPS), common in illness, trigger anorexia via inflammatory cytokines. These cytokines alter brain activity, affecting food intake and energy balance through various neural pathways.

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Area of Science:

Neuroscience
Immunology
Physiology

Background:

Anorexia is a key component of the acute-phase response to illness.
Microbial products like lipopolysaccharides (LPS) induce illness and anorexia via pro-inflammatory cytokines.
Cytokines mediate LPS effects through CD14 and toll-like receptor-4, impacting brain regions controlling appetite.

Purpose of the Study:

To elucidate the neural mechanisms underlying lipopolysaccharide (LPS)-induced anorexia.
To identify the role of cytokines, blood-brain barrier cells, and specific neurotransmitter systems in mediating appetite loss during illness.

Main Methods:

Review of existing literature on LPS-induced anorexia and immune signaling pathways.
Analysis of cytokine interactions with blood-brain barrier endothelial cells and perivascular cells.
Examination of the involvement of serotonergic, glucagon-like peptide-1, melanocortin, and orexin systems.

Main Results:

LPS-induced anorexia is primarily mediated by pro-inflammatory cytokines.
Cytokines act on blood-brain barrier cells to release messengers that influence neural activity.
Serotonin (5-HT), glucagon-like peptide-1, and the central melanocortin system are key mediators.
LPS reduce orexin expression and neuron activity, potentially contributing to inactivity and anorexia.

Conclusions:

Immune signaling pathways converge on central neural systems to regulate food intake and energy balance during illness.
Understanding these pathways is crucial for addressing anorexia associated with acute conditions.
The interplay between immune responses and neural circuits offers therapeutic targets for appetite regulation.