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An anti-inflammatory phenotype in visceral adipose tissue of old lean mice, augmented by exercise
Visceral adipose tissue is an immunogenic tissue, which turns detrimental during obesity by activation of proinflammatory macrophages. During aging, chronic inflammation increases proportional to visceral adipose tissue (VAT) mass and associates with escalating morbidity and mortality. Here, we util...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6700172/ https://www.ncbi.nlm.nih.gov/pubmed/31427677 http://dx.doi.org/10.1038/s41598-019-48587-2 |
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author | Ziegler, A. K. Damgaard, A. Mackey, A. L. Schjerling, P. Magnusson, P. Olesen, A. T. Kjaer, M. Scheele, C. |
author_facet | Ziegler, A. K. Damgaard, A. Mackey, A. L. Schjerling, P. Magnusson, P. Olesen, A. T. Kjaer, M. Scheele, C. |
author_sort | Ziegler, A. K. |
collection | PubMed |
description | Visceral adipose tissue is an immunogenic tissue, which turns detrimental during obesity by activation of proinflammatory macrophages. During aging, chronic inflammation increases proportional to visceral adipose tissue (VAT) mass and associates with escalating morbidity and mortality. Here, we utilize a mouse model to investigate the inflammatory status of visceral adipose tissue in lean aging mice and assess the effects of exercise training interventions. We randomized adult (11 months; n = 21) and old (23 months; n = 27) mice to resistance training (RT) or endurance training (ET), or to a sedentary control group (S). Strikingly, we observed an anti-inflammatory phenotype in the old mice, consisting of higher accumulation of M2 macrophages and IL-10 expression, compared to the adult mice. In concordance, old mice also had less VAT mass and smaller adipocytes compared to adult mice. In both age groups, exercise training enhanced the anti-inflammatory phenotype and increased PGC1-α mRNA expression. Intriguingly, the brown adipose tissue marker UCP1 was modestly higher in old mice, while remained unchanged by the intervention. In conclusion, in the absence of obesity, visceral adipose tissue possesses a pronounced anti-inflammatory phenotype during aging which is further enhanced by exercise. |
format | Online Article Text |
id | pubmed-6700172 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-67001722019-08-21 An anti-inflammatory phenotype in visceral adipose tissue of old lean mice, augmented by exercise Ziegler, A. K. Damgaard, A. Mackey, A. L. Schjerling, P. Magnusson, P. Olesen, A. T. Kjaer, M. Scheele, C. Sci Rep Article Visceral adipose tissue is an immunogenic tissue, which turns detrimental during obesity by activation of proinflammatory macrophages. During aging, chronic inflammation increases proportional to visceral adipose tissue (VAT) mass and associates with escalating morbidity and mortality. Here, we utilize a mouse model to investigate the inflammatory status of visceral adipose tissue in lean aging mice and assess the effects of exercise training interventions. We randomized adult (11 months; n = 21) and old (23 months; n = 27) mice to resistance training (RT) or endurance training (ET), or to a sedentary control group (S). Strikingly, we observed an anti-inflammatory phenotype in the old mice, consisting of higher accumulation of M2 macrophages and IL-10 expression, compared to the adult mice. In concordance, old mice also had less VAT mass and smaller adipocytes compared to adult mice. In both age groups, exercise training enhanced the anti-inflammatory phenotype and increased PGC1-α mRNA expression. Intriguingly, the brown adipose tissue marker UCP1 was modestly higher in old mice, while remained unchanged by the intervention. In conclusion, in the absence of obesity, visceral adipose tissue possesses a pronounced anti-inflammatory phenotype during aging which is further enhanced by exercise. Nature Publishing Group UK 2019-08-19 /pmc/articles/PMC6700172/ /pubmed/31427677 http://dx.doi.org/10.1038/s41598-019-48587-2 Text en © The Author(s) 2019 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 Ziegler, A. K. Damgaard, A. Mackey, A. L. Schjerling, P. Magnusson, P. Olesen, A. T. Kjaer, M. Scheele, C. An anti-inflammatory phenotype in visceral adipose tissue of old lean mice, augmented by exercise |
title | An anti-inflammatory phenotype in visceral adipose tissue of old lean mice, augmented by exercise |
title_full | An anti-inflammatory phenotype in visceral adipose tissue of old lean mice, augmented by exercise |
title_fullStr | An anti-inflammatory phenotype in visceral adipose tissue of old lean mice, augmented by exercise |
title_full_unstemmed | An anti-inflammatory phenotype in visceral adipose tissue of old lean mice, augmented by exercise |
title_short | An anti-inflammatory phenotype in visceral adipose tissue of old lean mice, augmented by exercise |
title_sort | anti-inflammatory phenotype in visceral adipose tissue of old lean mice, augmented by exercise |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6700172/ https://www.ncbi.nlm.nih.gov/pubmed/31427677 http://dx.doi.org/10.1038/s41598-019-48587-2 |
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