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iNOS promotes hypothalamic insulin resistance associated with deregulation of energy balance and obesity in rodents
Inducible nitric oxide (iNOS)-mediated S-nitrosation of the metabolic signaling pathway has emerged as a post-translational modification that triggers insulin resistance in obesity and aging. However, the effects of S-nitrosation in controlling energy homeostasis are unknown. Thus, in the present st...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5569114/ https://www.ncbi.nlm.nih.gov/pubmed/28835706 http://dx.doi.org/10.1038/s41598-017-08920-z |
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author | Katashima, Carlos Kiyoshi Silva, Vagner Ramon Rodrigues Lenhare, Luciene Marin, Rodrigo Miguel Carvalheira, José Barreto Campello |
author_facet | Katashima, Carlos Kiyoshi Silva, Vagner Ramon Rodrigues Lenhare, Luciene Marin, Rodrigo Miguel Carvalheira, José Barreto Campello |
author_sort | Katashima, Carlos Kiyoshi |
collection | PubMed |
description | Inducible nitric oxide (iNOS)-mediated S-nitrosation of the metabolic signaling pathway has emerged as a post-translational modification that triggers insulin resistance in obesity and aging. However, the effects of S-nitrosation in controlling energy homeostasis are unknown. Thus, in the present study we aimed to evaluate the effects of S-nitrosation in insulin signaling pathway in the hypothalamus of rodents. Herein, we demonstrated that the intracerebroventricular infusion of the nitric oxide (NO) donor S-nitrosoglutathione (GSNO) promoted hypothalamic insulin signaling resistance and replicated the food intake pattern of obese individuals. Indeed, obesity induced S-nitrosation of hypothalamic IR and Akt, whereas inhibition of iNOS or S-nitrosation of insulin signaling pathway protected against hypothalamic insulin resistance and normalized energy homeostasis. Overall, these findings indicated that S-nitrosation of insulin signaling pathway is required to sustain hypothalamic insulin resistance in obesity. |
format | Online Article Text |
id | pubmed-5569114 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-55691142017-09-01 iNOS promotes hypothalamic insulin resistance associated with deregulation of energy balance and obesity in rodents Katashima, Carlos Kiyoshi Silva, Vagner Ramon Rodrigues Lenhare, Luciene Marin, Rodrigo Miguel Carvalheira, José Barreto Campello Sci Rep Article Inducible nitric oxide (iNOS)-mediated S-nitrosation of the metabolic signaling pathway has emerged as a post-translational modification that triggers insulin resistance in obesity and aging. However, the effects of S-nitrosation in controlling energy homeostasis are unknown. Thus, in the present study we aimed to evaluate the effects of S-nitrosation in insulin signaling pathway in the hypothalamus of rodents. Herein, we demonstrated that the intracerebroventricular infusion of the nitric oxide (NO) donor S-nitrosoglutathione (GSNO) promoted hypothalamic insulin signaling resistance and replicated the food intake pattern of obese individuals. Indeed, obesity induced S-nitrosation of hypothalamic IR and Akt, whereas inhibition of iNOS or S-nitrosation of insulin signaling pathway protected against hypothalamic insulin resistance and normalized energy homeostasis. Overall, these findings indicated that S-nitrosation of insulin signaling pathway is required to sustain hypothalamic insulin resistance in obesity. Nature Publishing Group UK 2017-08-23 /pmc/articles/PMC5569114/ /pubmed/28835706 http://dx.doi.org/10.1038/s41598-017-08920-z Text en © The Author(s) 2017 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Katashima, Carlos Kiyoshi Silva, Vagner Ramon Rodrigues Lenhare, Luciene Marin, Rodrigo Miguel Carvalheira, José Barreto Campello iNOS promotes hypothalamic insulin resistance associated with deregulation of energy balance and obesity in rodents |
title | iNOS promotes hypothalamic insulin resistance associated with deregulation of energy balance and obesity in rodents |
title_full | iNOS promotes hypothalamic insulin resistance associated with deregulation of energy balance and obesity in rodents |
title_fullStr | iNOS promotes hypothalamic insulin resistance associated with deregulation of energy balance and obesity in rodents |
title_full_unstemmed | iNOS promotes hypothalamic insulin resistance associated with deregulation of energy balance and obesity in rodents |
title_short | iNOS promotes hypothalamic insulin resistance associated with deregulation of energy balance and obesity in rodents |
title_sort | inos promotes hypothalamic insulin resistance associated with deregulation of energy balance and obesity in rodents |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5569114/ https://www.ncbi.nlm.nih.gov/pubmed/28835706 http://dx.doi.org/10.1038/s41598-017-08920-z |
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