diethyl-maleate and Anorexia

diethyl-maleate has been researched along with Anorexia* in 1 studies

Other Studies

1 other study(ies) available for diethyl-maleate and Anorexia

Article	Year
Role for glutathione in the hyposensitivity of LPS-pretreated mice to LPS anorexia. European cytokine network, 2007, Volume: 18, Issue:2 To study the role of the redox state regulator glutathione (GSH) in bacterial lipopolysaccharide (LPS)-induced anorexia we measured total reduced GSH (trGSH) in liver, serum and brain in response to intraperitoneal (ip) lipopolysaccharide (LPS, 4 microg/mouse) injection in LPS-naïve and LPS-pretreated (4 microg/mouse given 3 days earlier) mice. LPS reduced food intake in LPS-naïve mice and LPS pretreatment attenuated this effect. LPS decreased trGSH at 24 hours after injection in LPS-naïve mice but 4 days later trGSH levels were upregulated in brain and liver, and this was associated with a significant attenuation of LPS-induced anorexia. In addition, LPS increased mitochondrial GSH levels in brain and liver at 4 days after injection. 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. Topics: Animals; Anorexia; Buthionine Sulfoximine; Glutathione; Interferon-gamma; Lipopolysaccharides; Liver; Male; Maleates; Mice; Mitochondria; Oxidation-Reduction; Reactive Oxygen Species; Tissue Distribution; Tumor Necrosis Factor-alpha	2007

Article

Year

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

European cytokine network, 2007, Volume: 18, Issue:2

To study the role of the redox state regulator glutathione (GSH) in bacterial lipopolysaccharide (LPS)-induced anorexia we measured total reduced GSH (trGSH) in liver, serum and brain in response to intraperitoneal (ip) lipopolysaccharide (LPS, 4 microg/mouse) injection in LPS-naïve and LPS-pretreated (4 microg/mouse given 3 days earlier) mice. LPS reduced food intake in LPS-naïve mice and LPS pretreatment attenuated this effect. LPS decreased trGSH at 24 hours after injection in LPS-naïve mice but 4 days later trGSH levels were upregulated in brain and liver, and this was associated with a significant attenuation of LPS-induced anorexia. In addition, LPS increased mitochondrial GSH levels in brain and liver at 4 days after injection. 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.

Topics: Animals; Anorexia; Buthionine Sulfoximine; Glutathione; Interferon-gamma; Lipopolysaccharides; Liver; Male; Maleates; Mice; Mitochondria; Oxidation-Reduction; Reactive Oxygen Species; Tissue Distribution; Tumor Necrosis Factor-alpha

2007