Richard, DenisDepartment of Anatomy and Physiology, Laval University, Quebec, Canada
Arsenijevic, DenisInstitute of Animal Sciences, ETH Zurich, Schwerzenbach, Switzerland - Division of Physiology, Department of Medicine, University of Fribourg, Switzerland
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.