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Oxidative phenotype induced by aerobic physical training prevents the obesity-linked insulin resistance without changes in gastrocnemius muscle ACE2-Angiotensin(1-7)-Mas axis
BACKGROUND: We investigate the effect of aerobic physical training (APT) on muscle morphofunctional markers and Angiotensin Converting Enzyme 2/Angiotensin 1-7/Mas receptor (ACE2/Ang 1-7/Mas) axis in an obesity-linked insulin resistance (IR) animal model induced by cafeteria diet (CAF). METHODS: Mal...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8262010/ https://www.ncbi.nlm.nih.gov/pubmed/34229719 http://dx.doi.org/10.1186/s13098-021-00693-w |
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author | Vecchiatto, Bruno da Silva, Rafael C. Higa, Talita S. Muller, Cynthia R. Américo, Anna Laura V. Fortunato-Lima, Vanessa C. Ferreira, Marília M. Martucci, Luiz Felipe Fonseca-Alaniz, Miriam H. Evangelista, Fabiana S. |
author_facet | Vecchiatto, Bruno da Silva, Rafael C. Higa, Talita S. Muller, Cynthia R. Américo, Anna Laura V. Fortunato-Lima, Vanessa C. Ferreira, Marília M. Martucci, Luiz Felipe Fonseca-Alaniz, Miriam H. Evangelista, Fabiana S. |
author_sort | Vecchiatto, Bruno |
collection | PubMed |
description | BACKGROUND: We investigate the effect of aerobic physical training (APT) on muscle morphofunctional markers and Angiotensin Converting Enzyme 2/Angiotensin 1-7/Mas receptor (ACE2/Ang 1-7/Mas) axis in an obesity-linked insulin resistance (IR) animal model induced by cafeteria diet (CAF). METHODS: Male C57BL/6J mice were assigned into groups CHOW-SED (chow diet, sedentary; n = 10), CHOW-TR (chow diet, trained; n = 10), CAF-SED (n = 10) and CAF-TR (n = 10). APT consisted in running sessions of 60 min at 60% of maximal speed, 5 days per week for 8 weeks. RESULTS: Trained groups had lower body weight and adiposity compared with sedentary groups. CAF-TR improved the glucose and insulin tolerance tests compared with CAF-SED group (AUC = 28.896 ± 1589 vs. 35.200 ± 1076 mg dL(−1) 120 min(−1); kITT = 4.1 ± 0.27 vs. 2.5 ± 0.28% min(−1), respectively). CHOW-TR and CAF-TR groups increased exercise tolerance, running intensity at which VO(2) max was reached, the expression of p-AMPK, p-ACC and PGC1-α proteins compared with CHOW-SED and CAF-SED. Mithocondrial protein expression of Mfn1, Mfn2 and Drp1 did not change. Lipid deposition reduced in CAF-TR compared with CAF-SED group (3.71 vs. 5.53%/area), but fiber typing, glycogen content, ACE2 activity, Ang 1-7 concentration and Mas receptor expression did not change. CONCLUSIONS: The APT prevents obesity-linked IR by modifying the skeletal muscle phenotype to one more oxidative independent of changes in the muscle ACE2/Ang 1-7/Mas axis. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s13098-021-00693-w. |
format | Online Article Text |
id | pubmed-8262010 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-82620102021-07-07 Oxidative phenotype induced by aerobic physical training prevents the obesity-linked insulin resistance without changes in gastrocnemius muscle ACE2-Angiotensin(1-7)-Mas axis Vecchiatto, Bruno da Silva, Rafael C. Higa, Talita S. Muller, Cynthia R. Américo, Anna Laura V. Fortunato-Lima, Vanessa C. Ferreira, Marília M. Martucci, Luiz Felipe Fonseca-Alaniz, Miriam H. Evangelista, Fabiana S. Diabetol Metab Syndr Research BACKGROUND: We investigate the effect of aerobic physical training (APT) on muscle morphofunctional markers and Angiotensin Converting Enzyme 2/Angiotensin 1-7/Mas receptor (ACE2/Ang 1-7/Mas) axis in an obesity-linked insulin resistance (IR) animal model induced by cafeteria diet (CAF). METHODS: Male C57BL/6J mice were assigned into groups CHOW-SED (chow diet, sedentary; n = 10), CHOW-TR (chow diet, trained; n = 10), CAF-SED (n = 10) and CAF-TR (n = 10). APT consisted in running sessions of 60 min at 60% of maximal speed, 5 days per week for 8 weeks. RESULTS: Trained groups had lower body weight and adiposity compared with sedentary groups. CAF-TR improved the glucose and insulin tolerance tests compared with CAF-SED group (AUC = 28.896 ± 1589 vs. 35.200 ± 1076 mg dL(−1) 120 min(−1); kITT = 4.1 ± 0.27 vs. 2.5 ± 0.28% min(−1), respectively). CHOW-TR and CAF-TR groups increased exercise tolerance, running intensity at which VO(2) max was reached, the expression of p-AMPK, p-ACC and PGC1-α proteins compared with CHOW-SED and CAF-SED. Mithocondrial protein expression of Mfn1, Mfn2 and Drp1 did not change. Lipid deposition reduced in CAF-TR compared with CAF-SED group (3.71 vs. 5.53%/area), but fiber typing, glycogen content, ACE2 activity, Ang 1-7 concentration and Mas receptor expression did not change. CONCLUSIONS: The APT prevents obesity-linked IR by modifying the skeletal muscle phenotype to one more oxidative independent of changes in the muscle ACE2/Ang 1-7/Mas axis. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s13098-021-00693-w. BioMed Central 2021-07-06 /pmc/articles/PMC8262010/ /pubmed/34229719 http://dx.doi.org/10.1186/s13098-021-00693-w Text en © The Author(s) 2021 https://creativecommons.org/licenses/by/4.0/Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data. |
spellingShingle | Research Vecchiatto, Bruno da Silva, Rafael C. Higa, Talita S. Muller, Cynthia R. Américo, Anna Laura V. Fortunato-Lima, Vanessa C. Ferreira, Marília M. Martucci, Luiz Felipe Fonseca-Alaniz, Miriam H. Evangelista, Fabiana S. Oxidative phenotype induced by aerobic physical training prevents the obesity-linked insulin resistance without changes in gastrocnemius muscle ACE2-Angiotensin(1-7)-Mas axis |
title | Oxidative phenotype induced by aerobic physical training prevents the obesity-linked insulin resistance without changes in gastrocnemius muscle ACE2-Angiotensin(1-7)-Mas axis |
title_full | Oxidative phenotype induced by aerobic physical training prevents the obesity-linked insulin resistance without changes in gastrocnemius muscle ACE2-Angiotensin(1-7)-Mas axis |
title_fullStr | Oxidative phenotype induced by aerobic physical training prevents the obesity-linked insulin resistance without changes in gastrocnemius muscle ACE2-Angiotensin(1-7)-Mas axis |
title_full_unstemmed | Oxidative phenotype induced by aerobic physical training prevents the obesity-linked insulin resistance without changes in gastrocnemius muscle ACE2-Angiotensin(1-7)-Mas axis |
title_short | Oxidative phenotype induced by aerobic physical training prevents the obesity-linked insulin resistance without changes in gastrocnemius muscle ACE2-Angiotensin(1-7)-Mas axis |
title_sort | oxidative phenotype induced by aerobic physical training prevents the obesity-linked insulin resistance without changes in gastrocnemius muscle ace2-angiotensin(1-7)-mas axis |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8262010/ https://www.ncbi.nlm.nih.gov/pubmed/34229719 http://dx.doi.org/10.1186/s13098-021-00693-w |
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