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Intermittent prednisone treatment in mice promotes exercise tolerance in obesity through adiponectin
The fat–muscle communication regulates metabolism and involves circulating signals like adiponectin. Modulation of this cross-talk could benefit muscle bioenergetics and exercise tolerance in conditions like obesity. Chronic daily intake of exogenous glucocorticoids produces or exacerbates metabolic...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Rockefeller University Press
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8980841/ https://www.ncbi.nlm.nih.gov/pubmed/35363257 http://dx.doi.org/10.1084/jem.20211906 |
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author | Quattrocelli, Mattia Wintzinger, Michelle Miz, Karen Panta, Manoj Prabakaran, Ashok D. Barish, Grant D. Chandel, Navdeep S. McNally, Elizabeth M. |
author_facet | Quattrocelli, Mattia Wintzinger, Michelle Miz, Karen Panta, Manoj Prabakaran, Ashok D. Barish, Grant D. Chandel, Navdeep S. McNally, Elizabeth M. |
author_sort | Quattrocelli, Mattia |
collection | PubMed |
description | The fat–muscle communication regulates metabolism and involves circulating signals like adiponectin. Modulation of this cross-talk could benefit muscle bioenergetics and exercise tolerance in conditions like obesity. Chronic daily intake of exogenous glucocorticoids produces or exacerbates metabolic stress, often leading to obesity. In stark contrast to the daily intake, we discovered that intermittent pulses of glucocorticoids improve dystrophic muscle metabolism. However, the underlying mechanisms, particularly in the context of obesity, are still largely unknown. Here we report that in mice with diet-induced obesity, intermittent once-weekly prednisone increased total and high-molecular weight adiponectin levels and improved exercise tolerance and energy expenditure. These effects were dependent upon adiponectin, as shown by genetic ablation of the adipokine. Upregulation of Adipoq occurred through the glucocorticoid receptor (GR), as this effect was blocked by inducible GR ablation in adipocytes. The treatment increased the muscle metabolic response of adiponectin through the CAMKK2–AMPK cascade. Our study demonstrates that intermittent glucocorticoids produce healthful metabolic remodeling in diet-induced obesity. |
format | Online Article Text |
id | pubmed-8980841 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-89808412022-11-01 Intermittent prednisone treatment in mice promotes exercise tolerance in obesity through adiponectin Quattrocelli, Mattia Wintzinger, Michelle Miz, Karen Panta, Manoj Prabakaran, Ashok D. Barish, Grant D. Chandel, Navdeep S. McNally, Elizabeth M. J Exp Med Brief Definitive Report The fat–muscle communication regulates metabolism and involves circulating signals like adiponectin. Modulation of this cross-talk could benefit muscle bioenergetics and exercise tolerance in conditions like obesity. Chronic daily intake of exogenous glucocorticoids produces or exacerbates metabolic stress, often leading to obesity. In stark contrast to the daily intake, we discovered that intermittent pulses of glucocorticoids improve dystrophic muscle metabolism. However, the underlying mechanisms, particularly in the context of obesity, are still largely unknown. Here we report that in mice with diet-induced obesity, intermittent once-weekly prednisone increased total and high-molecular weight adiponectin levels and improved exercise tolerance and energy expenditure. These effects were dependent upon adiponectin, as shown by genetic ablation of the adipokine. Upregulation of Adipoq occurred through the glucocorticoid receptor (GR), as this effect was blocked by inducible GR ablation in adipocytes. The treatment increased the muscle metabolic response of adiponectin through the CAMKK2–AMPK cascade. Our study demonstrates that intermittent glucocorticoids produce healthful metabolic remodeling in diet-induced obesity. Rockefeller University Press 2022-04-01 /pmc/articles/PMC8980841/ /pubmed/35363257 http://dx.doi.org/10.1084/jem.20211906 Text en © 2022 Quattrocelli et al. https://creativecommons.org/licenses/by-nc-sa/4.0/http://www.rupress.org/terms/This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms/). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 International license, as described at https://creativecommons.org/licenses/by-nc-sa/4.0/). |
spellingShingle | Brief Definitive Report Quattrocelli, Mattia Wintzinger, Michelle Miz, Karen Panta, Manoj Prabakaran, Ashok D. Barish, Grant D. Chandel, Navdeep S. McNally, Elizabeth M. Intermittent prednisone treatment in mice promotes exercise tolerance in obesity through adiponectin |
title | Intermittent prednisone treatment in mice promotes exercise tolerance in obesity through adiponectin |
title_full | Intermittent prednisone treatment in mice promotes exercise tolerance in obesity through adiponectin |
title_fullStr | Intermittent prednisone treatment in mice promotes exercise tolerance in obesity through adiponectin |
title_full_unstemmed | Intermittent prednisone treatment in mice promotes exercise tolerance in obesity through adiponectin |
title_short | Intermittent prednisone treatment in mice promotes exercise tolerance in obesity through adiponectin |
title_sort | intermittent prednisone treatment in mice promotes exercise tolerance in obesity through adiponectin |
topic | Brief Definitive Report |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8980841/ https://www.ncbi.nlm.nih.gov/pubmed/35363257 http://dx.doi.org/10.1084/jem.20211906 |
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