Open Access

ARTICLE

Role for glutathione in the hyposensitivity of LPS-pretreated mice to LPS anorexia

Noemi Hernadfalvi¹, Wolfgang Langhans¹, Claudia von Meyenburg¹, Brigitte Onteniente², Denis Richard³, Denis Arsenijevic¹

1 Institute of Animal Sciences, ETH Zurich, Schwerzenbach, Switzerland
2 INSERM UMR421, Creteil, France
3 Department of Anatomy and Physiology, Laval University, Quebec, Canada

* Corresponding Author: Denis Arsenijevic,

European Cytokine Network 2007, 18(2), 39-45. https://doi.org/10.1684/ecn.2007.0090

Abstract

To study the role of the redox state regulator glutathione (GSH) in bacterial lipopolysaccharide (LPS)-induced anorexia we measured GSH in liver, serum and brain in response to intraperitoneal (ip) lipopolysaccharide (LPS, 4lg/mouse) injection in LPS-naïve and LPS-pretreated (4 lg/mouse) mice. LPS reduced food intake in LPS-naïve mice and LPS pretreatment attenuated this effect. LPS reduced total reduced GSH at 24 hours after injection in LPS-naïve mice. On the other hand, LPS pretreatment caused an upregulation of GSH levels in brain and liver, and this was associated with a significant attenuation of LPS-induced anorexia. In addition, LPS pretreatment increased mitochondrial GSH levels in brain and liver. Pharmacological GSH depletion with diethylmaleate and L-buthionine sulfoximine in LPS-pretreated mice ablated the hyposensitivity to the anorexic effect of LPS. Together, these findings suggest a prominent role for GSH and its intracellular repartition in LPS anorexia.

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