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A possible association between fructose consumption and pulmonary emphysema
Chronic Obstructive Pulmonary Disease (COPD) is a syndrome that comprises several distinct and overlapping phenotypes. In addition to persistent airflow limitation and respiratory symptoms, COPD is also characterized by chronic systemic inflammation. Epidemiological studies have shown that dietary f...
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/PMC6597575/ https://www.ncbi.nlm.nih.gov/pubmed/31249347 http://dx.doi.org/10.1038/s41598-019-45594-1 |
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author | Suehiro, Camila Liyoko Toledo-Arruda, Alessandra Choqueta de Vieira, Rodolfo de Paula Almeida, Francine Maria de Olivo, Clarice Rosa Martins, Milton de Arruda Lin, Chin Jia |
author_facet | Suehiro, Camila Liyoko Toledo-Arruda, Alessandra Choqueta de Vieira, Rodolfo de Paula Almeida, Francine Maria de Olivo, Clarice Rosa Martins, Milton de Arruda Lin, Chin Jia |
author_sort | Suehiro, Camila Liyoko |
collection | PubMed |
description | Chronic Obstructive Pulmonary Disease (COPD) is a syndrome that comprises several distinct and overlapping phenotypes. In addition to persistent airflow limitation and respiratory symptoms, COPD is also characterized by chronic systemic inflammation. Epidemiological studies have shown that dietary fibers, fruits and vegetables intake protects against the COPD development, while fructose-loading is associated with increased risk of asthma and chronic bronchitis. Since dietary factors might affect susceptibility to COPD by modulating oxidative stress and inflammatory responses, we evaluated how fructose feeding might affect the smoking-induced emphysema in mice. We found that chronic fructose intake induced destruction and remodeling of lung parenchyma and impairment of respiratory mechanics, which are associated with distinctive cytokine profiles in bronchoalveolar lavage fluid, blood plasma and skeletal muscle. The combined effects of chronic fructose intake and cigarette smoking on destruction of lung parenchyma are more pronounced than the effects of either alone. Excessive intake of fructose might directly cause pulmonary emphysema in mice rather than just altering its natural history by facilitating the installation of a low-grade systemic inflammatory milieu. |
format | Online Article Text |
id | pubmed-6597575 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-65975752019-07-09 A possible association between fructose consumption and pulmonary emphysema Suehiro, Camila Liyoko Toledo-Arruda, Alessandra Choqueta de Vieira, Rodolfo de Paula Almeida, Francine Maria de Olivo, Clarice Rosa Martins, Milton de Arruda Lin, Chin Jia Sci Rep Article Chronic Obstructive Pulmonary Disease (COPD) is a syndrome that comprises several distinct and overlapping phenotypes. In addition to persistent airflow limitation and respiratory symptoms, COPD is also characterized by chronic systemic inflammation. Epidemiological studies have shown that dietary fibers, fruits and vegetables intake protects against the COPD development, while fructose-loading is associated with increased risk of asthma and chronic bronchitis. Since dietary factors might affect susceptibility to COPD by modulating oxidative stress and inflammatory responses, we evaluated how fructose feeding might affect the smoking-induced emphysema in mice. We found that chronic fructose intake induced destruction and remodeling of lung parenchyma and impairment of respiratory mechanics, which are associated with distinctive cytokine profiles in bronchoalveolar lavage fluid, blood plasma and skeletal muscle. The combined effects of chronic fructose intake and cigarette smoking on destruction of lung parenchyma are more pronounced than the effects of either alone. Excessive intake of fructose might directly cause pulmonary emphysema in mice rather than just altering its natural history by facilitating the installation of a low-grade systemic inflammatory milieu. Nature Publishing Group UK 2019-06-27 /pmc/articles/PMC6597575/ /pubmed/31249347 http://dx.doi.org/10.1038/s41598-019-45594-1 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 Suehiro, Camila Liyoko Toledo-Arruda, Alessandra Choqueta de Vieira, Rodolfo de Paula Almeida, Francine Maria de Olivo, Clarice Rosa Martins, Milton de Arruda Lin, Chin Jia A possible association between fructose consumption and pulmonary emphysema |
title | A possible association between fructose consumption and pulmonary emphysema |
title_full | A possible association between fructose consumption and pulmonary emphysema |
title_fullStr | A possible association between fructose consumption and pulmonary emphysema |
title_full_unstemmed | A possible association between fructose consumption and pulmonary emphysema |
title_short | A possible association between fructose consumption and pulmonary emphysema |
title_sort | possible association between fructose consumption and pulmonary emphysema |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6597575/ https://www.ncbi.nlm.nih.gov/pubmed/31249347 http://dx.doi.org/10.1038/s41598-019-45594-1 |
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