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Involvement of nitric oxide in disease-related anorexia


Cordani, C. Involvement of nitric oxide in disease-related anorexia. 2010, University of Zurich, Vetsuisse Faculty.

Abstract

The nitric oxide (NO) producing enzyme inducible NO synthase isoform (iNOS) is strongly upregulated under inflammatory conditions in the arcuate nucleus, a hypothalamic key structure for the control of food intake and energy balance. This project aims to prove the concept that a pharmacological blockade of iNOS attenuates anorexia and associated disease symptoms induced by the proinflammatory endotoxin lipopolysaccharide (LPS). We also analyzed the association between LPS-induced anorexia and pSTAT3-formation in the arcuate nucleus and in hindbrain feeding centers (AP/NTS region). pSTAT3 is a cytokine dependent transcription factor, which is suggested to control iNOS expression. Findings and conclusions: NO contributes to LPS-induced anorexia because anorexia is attenuated by the specific iNOS-inhibitor 1400W. In addition, 1400W treatment also ameliorates other LPS-induced symptoms (e.g. adipsia, fever, inactivity). LPS treatment induces a time-dependent pSTAT3 formation in the ARC and the AP/NTS region of rats; this parallels the time course of LPS anorexia. LPS does not induce a pSTAT3 response in LPS tolerant rats that do not show an anorectic LPS response either. These findings provide evidence that NO is involved in disease-related anorexia and that pharmacological iNOS blockade may be a therapeutic approach to treat sickness anorexia/cachexia. LPS anorexia is associated with enhanced pSTAT3 signaling. Which might be involved in the underlying transcriptional mechanisms.

The nitric oxide (NO) producing enzyme inducible NO synthase isoform (iNOS) is strongly upregulated under inflammatory conditions in the arcuate nucleus, a hypothalamic key structure for the control of food intake and energy balance. This project aims to prove the concept that a pharmacological blockade of iNOS attenuates anorexia and associated disease symptoms induced by the proinflammatory endotoxin lipopolysaccharide (LPS). We also analyzed the association between LPS-induced anorexia and pSTAT3-formation in the arcuate nucleus and in hindbrain feeding centers (AP/NTS region). pSTAT3 is a cytokine dependent transcription factor, which is suggested to control iNOS expression. Findings and conclusions: NO contributes to LPS-induced anorexia because anorexia is attenuated by the specific iNOS-inhibitor 1400W. In addition, 1400W treatment also ameliorates other LPS-induced symptoms (e.g. adipsia, fever, inactivity). LPS treatment induces a time-dependent pSTAT3 formation in the ARC and the AP/NTS region of rats; this parallels the time course of LPS anorexia. LPS does not induce a pSTAT3 response in LPS tolerant rats that do not show an anorectic LPS response either. These findings provide evidence that NO is involved in disease-related anorexia and that pharmacological iNOS blockade may be a therapeutic approach to treat sickness anorexia/cachexia. LPS anorexia is associated with enhanced pSTAT3 signaling. Which might be involved in the underlying transcriptional mechanisms.

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Additional indexing

Item Type:Dissertation
Referees:Riediger T, Schmid H
Communities & Collections:05 Vetsuisse Faculty > Institute of Veterinary Physiology
Dewey Decimal Classification:570 Life sciences; biology
Language:English
Date:2010
Deposited On:08 Jun 2010 17:51
Last Modified:14 Sep 2016 13:43
Number of Pages:51
Permanent URL: https://doi.org/10.5167/uzh-34219

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