Role for glutathione in the hyposensitivity of LPS-pretreated mice to LPS anorexia
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Hernadfalvi, Noemi
Institute of Animal Sciences, ETH Zurich, Schwerzenbach, Switzerland
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Langhans, Wolfgang
Institute of Animal Sciences, ETH Zurich, Schwerzenbach, Switzerland
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Meyenburg, Claudia von
Institute of Animal Sciences, ETH Zurich, Schwerzenbach, Switzerland
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Onteniente, Brigitte
INSERM UMR421, Creteil, France
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Richard, Denis
Department of Anatomy and Physiology, Laval University, Quebec, Canada
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Arsenijevic, Denis
Institute of Animal Sciences, ETH Zurich, Schwerzenbach, Switzerland - Division of Physiology, Department of Medicine, University of Fribourg, Switzerland
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Published in:
- European Cytokine Network. - 2007, vol. 18, no. 2, p. 39-45
English
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, 4μg/mouse) injection in LPS-naïve and LPS-pretreated (4 μg/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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Faculty
- Faculté des sciences et de médecine
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Department
- Département de Médecine
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Language
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Classification
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Biological sciences
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License
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License undefined
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Identifiers
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Persistent URL
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https://folia.unifr.ch/unifr/documents/300578
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