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Oleoylethanolamide‐induced anorexia in rats is associated with locomotor impairment
The endogenous peroxisome proliferator‐activated receptor alpha (PPAR‐α) agonist Oleoylethanolamide (OEA) inhibits eating in rodents, mainly by delaying the onset of meals. The underlying mechanisms of OEA‐induced anorexia, however, remain unclear. Animals treated with high OEA doses were shown to d...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5817840/ https://www.ncbi.nlm.nih.gov/pubmed/29388342 http://dx.doi.org/10.14814/phy2.13517 |
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author | Fedele, Shahana Arnold, Myrtha Krieger, Jean‐Philippe Wolfstädter, Bernd Meyer, Urs Langhans, Wolfgang Mansouri, Abdelhak |
author_facet | Fedele, Shahana Arnold, Myrtha Krieger, Jean‐Philippe Wolfstädter, Bernd Meyer, Urs Langhans, Wolfgang Mansouri, Abdelhak |
author_sort | Fedele, Shahana |
collection | PubMed |
description | The endogenous peroxisome proliferator‐activated receptor alpha (PPAR‐α) agonist Oleoylethanolamide (OEA) inhibits eating in rodents, mainly by delaying the onset of meals. The underlying mechanisms of OEA‐induced anorexia, however, remain unclear. Animals treated with high OEA doses were shown to display signs of discomfort and impaired locomotion. Therefore, we first examined whether the impaired locomotion may contribute to OEA's anorectic effect. Second, it is controversial whether abdominal vagal afferents are necessary for OEA's anorectic effect. Thus, we explored alternative peripheral neural pathways mediating IP OEA's anorectic effect by performing a celiac‐superior mesenteric ganglionectomy (CGX) or a subdiaphragmatic vagal deafferentation (SDA) alone or in combination. Exogenously administered OEA at a commonly used dose (10 mg/kg BW, IP) concurrently reduced food intake and compromised locomotor activity. Attempts to dissociate both phenomena using the dopamine D2/D3 receptor agonist Quinpirole (1 mg/kg BW, SC) failed because Quinpirole antagonized both, OEA‐induced locomotor impairment and delay in eating onset. CGX attenuated the prolongation of the latency to eat by IP OEA, but neither SDA nor CGX prevented IP OEA‐induced locomotor impairment. Our results indicate that IP OEA's anorectic effect may be secondary to impaired locomotion rather than due to physiological satiety. They further confirm that vagal afferents do not mediate exogenous OEA's anorectic effects, but suggest a role for spinal afferents in addition to an alternative, nonneuronal signaling route. |
format | Online Article Text |
id | pubmed-5817840 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-58178402018-03-15 Oleoylethanolamide‐induced anorexia in rats is associated with locomotor impairment Fedele, Shahana Arnold, Myrtha Krieger, Jean‐Philippe Wolfstädter, Bernd Meyer, Urs Langhans, Wolfgang Mansouri, Abdelhak Physiol Rep Original Research The endogenous peroxisome proliferator‐activated receptor alpha (PPAR‐α) agonist Oleoylethanolamide (OEA) inhibits eating in rodents, mainly by delaying the onset of meals. The underlying mechanisms of OEA‐induced anorexia, however, remain unclear. Animals treated with high OEA doses were shown to display signs of discomfort and impaired locomotion. Therefore, we first examined whether the impaired locomotion may contribute to OEA's anorectic effect. Second, it is controversial whether abdominal vagal afferents are necessary for OEA's anorectic effect. Thus, we explored alternative peripheral neural pathways mediating IP OEA's anorectic effect by performing a celiac‐superior mesenteric ganglionectomy (CGX) or a subdiaphragmatic vagal deafferentation (SDA) alone or in combination. Exogenously administered OEA at a commonly used dose (10 mg/kg BW, IP) concurrently reduced food intake and compromised locomotor activity. Attempts to dissociate both phenomena using the dopamine D2/D3 receptor agonist Quinpirole (1 mg/kg BW, SC) failed because Quinpirole antagonized both, OEA‐induced locomotor impairment and delay in eating onset. CGX attenuated the prolongation of the latency to eat by IP OEA, but neither SDA nor CGX prevented IP OEA‐induced locomotor impairment. Our results indicate that IP OEA's anorectic effect may be secondary to impaired locomotion rather than due to physiological satiety. They further confirm that vagal afferents do not mediate exogenous OEA's anorectic effects, but suggest a role for spinal afferents in addition to an alternative, nonneuronal signaling route. John Wiley and Sons Inc. 2018-02-01 /pmc/articles/PMC5817840/ /pubmed/29388342 http://dx.doi.org/10.14814/phy2.13517 Text en © 2018 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society This is an open access article under the terms of the Creative Commons Attribution (http://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Research Fedele, Shahana Arnold, Myrtha Krieger, Jean‐Philippe Wolfstädter, Bernd Meyer, Urs Langhans, Wolfgang Mansouri, Abdelhak Oleoylethanolamide‐induced anorexia in rats is associated with locomotor impairment |
title | Oleoylethanolamide‐induced anorexia in rats is associated with locomotor impairment |
title_full | Oleoylethanolamide‐induced anorexia in rats is associated with locomotor impairment |
title_fullStr | Oleoylethanolamide‐induced anorexia in rats is associated with locomotor impairment |
title_full_unstemmed | Oleoylethanolamide‐induced anorexia in rats is associated with locomotor impairment |
title_short | Oleoylethanolamide‐induced anorexia in rats is associated with locomotor impairment |
title_sort | oleoylethanolamide‐induced anorexia in rats is associated with locomotor impairment |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5817840/ https://www.ncbi.nlm.nih.gov/pubmed/29388342 http://dx.doi.org/10.14814/phy2.13517 |
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