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Exercise training modulates the gut microbiota profile and impairs inflammatory signaling pathways in obese children

Childhood obesity has reached epidemic levels and is a serious health concern associated with metabolic syndrome, nonalcoholic fatty liver disease, and gut microbiota alterations. Physical exercise is known to counteract obesity progression and modulate the gut microbiota composition. This study aim...

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Autores principales: Quiroga, Rocío, Nistal, Esther, Estébanez, Brisamar, Porras, David, Juárez-Fernández, María, Martínez-Flórez, Susana, García-Mediavilla, María Victoria, de Paz, José A., González-Gallego, Javier, Sánchez-Campos, Sonia, Cuevas, María J.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8080668/
https://www.ncbi.nlm.nih.gov/pubmed/32624568
http://dx.doi.org/10.1038/s12276-020-0459-0
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author Quiroga, Rocío
Nistal, Esther
Estébanez, Brisamar
Porras, David
Juárez-Fernández, María
Martínez-Flórez, Susana
García-Mediavilla, María Victoria
de Paz, José A.
González-Gallego, Javier
Sánchez-Campos, Sonia
Cuevas, María J.
author_facet Quiroga, Rocío
Nistal, Esther
Estébanez, Brisamar
Porras, David
Juárez-Fernández, María
Martínez-Flórez, Susana
García-Mediavilla, María Victoria
de Paz, José A.
González-Gallego, Javier
Sánchez-Campos, Sonia
Cuevas, María J.
author_sort Quiroga, Rocío
collection PubMed
description Childhood obesity has reached epidemic levels and is a serious health concern associated with metabolic syndrome, nonalcoholic fatty liver disease, and gut microbiota alterations. Physical exercise is known to counteract obesity progression and modulate the gut microbiota composition. This study aims to determine the effect of a 12-week strength and endurance combined training program on gut microbiota and inflammation in obese pediatric patients. Thirty-nine obese children were assigned randomly to the control or training group. Anthropometric and biochemical parameters, muscular strength, and inflammatory signaling pathways in mononuclear cells were evaluated. Bacterial composition and functionality were determined by massive sequencing and metabolomic analysis. Exercise reduced plasma glucose levels and increased dynamic strength in the upper and lower extremities compared with the obese control group. Metagenomic analysis revealed a bacterial composition associated with obesity, showing changes at the phylum, class, and genus levels. Exercise counteracted this profile, significantly reducing the Proteobacteria phylum and Gammaproteobacteria class. Moreover, physical activity tended to increase some genera, such as Blautia, Dialister, and Roseburia, leading to a microbiota profile similar to that of healthy children. Metabolomic analysis revealed changes in short-chain fatty acids, branched-chain amino acids, and several sugars in response to exercise, in correlation with a specific microbiota profile. Finally, the training protocol significantly inhibited the activation of the obesity-associated NLRP3 signaling pathway. Our data suggest the existence of an obesity-related deleterious microbiota profile that is positively modified by physical activity intervention. Exercise training could be considered an efficient nonpharmacological therapy, reducing inflammatory signaling pathways induced by obesity in children via microbiota modulation.
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spelling pubmed-80806682021-04-29 Exercise training modulates the gut microbiota profile and impairs inflammatory signaling pathways in obese children Quiroga, Rocío Nistal, Esther Estébanez, Brisamar Porras, David Juárez-Fernández, María Martínez-Flórez, Susana García-Mediavilla, María Victoria de Paz, José A. González-Gallego, Javier Sánchez-Campos, Sonia Cuevas, María J. Exp Mol Med Article Childhood obesity has reached epidemic levels and is a serious health concern associated with metabolic syndrome, nonalcoholic fatty liver disease, and gut microbiota alterations. Physical exercise is known to counteract obesity progression and modulate the gut microbiota composition. This study aims to determine the effect of a 12-week strength and endurance combined training program on gut microbiota and inflammation in obese pediatric patients. Thirty-nine obese children were assigned randomly to the control or training group. Anthropometric and biochemical parameters, muscular strength, and inflammatory signaling pathways in mononuclear cells were evaluated. Bacterial composition and functionality were determined by massive sequencing and metabolomic analysis. Exercise reduced plasma glucose levels and increased dynamic strength in the upper and lower extremities compared with the obese control group. Metagenomic analysis revealed a bacterial composition associated with obesity, showing changes at the phylum, class, and genus levels. Exercise counteracted this profile, significantly reducing the Proteobacteria phylum and Gammaproteobacteria class. Moreover, physical activity tended to increase some genera, such as Blautia, Dialister, and Roseburia, leading to a microbiota profile similar to that of healthy children. Metabolomic analysis revealed changes in short-chain fatty acids, branched-chain amino acids, and several sugars in response to exercise, in correlation with a specific microbiota profile. Finally, the training protocol significantly inhibited the activation of the obesity-associated NLRP3 signaling pathway. Our data suggest the existence of an obesity-related deleterious microbiota profile that is positively modified by physical activity intervention. Exercise training could be considered an efficient nonpharmacological therapy, reducing inflammatory signaling pathways induced by obesity in children via microbiota modulation. Nature Publishing Group UK 2020-07-06 /pmc/articles/PMC8080668/ /pubmed/32624568 http://dx.doi.org/10.1038/s12276-020-0459-0 Text en © The Author(s) 2020 https://creativecommons.org/licenses/by/4.0/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/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Article
Quiroga, Rocío
Nistal, Esther
Estébanez, Brisamar
Porras, David
Juárez-Fernández, María
Martínez-Flórez, Susana
García-Mediavilla, María Victoria
de Paz, José A.
González-Gallego, Javier
Sánchez-Campos, Sonia
Cuevas, María J.
Exercise training modulates the gut microbiota profile and impairs inflammatory signaling pathways in obese children
title Exercise training modulates the gut microbiota profile and impairs inflammatory signaling pathways in obese children
title_full Exercise training modulates the gut microbiota profile and impairs inflammatory signaling pathways in obese children
title_fullStr Exercise training modulates the gut microbiota profile and impairs inflammatory signaling pathways in obese children
title_full_unstemmed Exercise training modulates the gut microbiota profile and impairs inflammatory signaling pathways in obese children
title_short Exercise training modulates the gut microbiota profile and impairs inflammatory signaling pathways in obese children
title_sort exercise training modulates the gut microbiota profile and impairs inflammatory signaling pathways in obese children
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8080668/
https://www.ncbi.nlm.nih.gov/pubmed/32624568
http://dx.doi.org/10.1038/s12276-020-0459-0
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