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Exercise Training but not Curcumin Supplementation Decreases Immune Cell Infiltration in the Pancreatic Islets of a Genetically Susceptible Model of Type 1 Diabetes
BACKGROUND: The main mechanism involved in the pathogenesis of autoimmunity is an uncontrolled inflammatory response against self-antigens. Therefore, anti-inflammatory factors, such as the intake of bioactive compounds and a physically active lifestyle, may decrease or cease the development of auto...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer International Publishing
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5380567/ https://www.ncbi.nlm.nih.gov/pubmed/28378202 http://dx.doi.org/10.1186/s40798-017-0082-3 |
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author | Oharomari, Leandro Kansuke de Moraes, Camila Navarro, Anderson Marliere |
author_facet | Oharomari, Leandro Kansuke de Moraes, Camila Navarro, Anderson Marliere |
author_sort | Oharomari, Leandro Kansuke |
collection | PubMed |
description | BACKGROUND: The main mechanism involved in the pathogenesis of autoimmunity is an uncontrolled inflammatory response against self-antigens. Therefore, anti-inflammatory factors, such as the intake of bioactive compounds and a physically active lifestyle, may decrease or cease the development of autoimmune diseases. Type 1 diabetes (T1D) is an autoimmune disease characterized by pancreatic β cell destruction. The non-obese diabetic (NOD) mouse is a model of spontaneous T1D and is the model most similar to human disease. METHODS: To determine the effects of exercise training and curcumin supplementation on T1D progression, 48 NOD mice, 5 weeks old, were randomly divided into four groups: control, curcumin supplementation, trained, and trained plus curcumin. Every 2 weeks, blood glucose was measured using a glucometer. At the end of 20 weeks, a histopathological procedure was used to assess immune cells infiltration into pancreatic β cells (insulitis). RESULTS: Moderate intensity exercise training has the potential to protect pancreatic β cells against an immune response in vivo. However, curcumin supplementation failed to attenuate insulitis in NOD mice. CONCLUSIONS: These data provide evidence that exercise training can mitigate T1D development in genetically susceptible mice. |
format | Online Article Text |
id | pubmed-5380567 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Springer International Publishing |
record_format | MEDLINE/PubMed |
spelling | pubmed-53805672017-04-20 Exercise Training but not Curcumin Supplementation Decreases Immune Cell Infiltration in the Pancreatic Islets of a Genetically Susceptible Model of Type 1 Diabetes Oharomari, Leandro Kansuke de Moraes, Camila Navarro, Anderson Marliere Sports Med Open Original Research Article BACKGROUND: The main mechanism involved in the pathogenesis of autoimmunity is an uncontrolled inflammatory response against self-antigens. Therefore, anti-inflammatory factors, such as the intake of bioactive compounds and a physically active lifestyle, may decrease or cease the development of autoimmune diseases. Type 1 diabetes (T1D) is an autoimmune disease characterized by pancreatic β cell destruction. The non-obese diabetic (NOD) mouse is a model of spontaneous T1D and is the model most similar to human disease. METHODS: To determine the effects of exercise training and curcumin supplementation on T1D progression, 48 NOD mice, 5 weeks old, were randomly divided into four groups: control, curcumin supplementation, trained, and trained plus curcumin. Every 2 weeks, blood glucose was measured using a glucometer. At the end of 20 weeks, a histopathological procedure was used to assess immune cells infiltration into pancreatic β cells (insulitis). RESULTS: Moderate intensity exercise training has the potential to protect pancreatic β cells against an immune response in vivo. However, curcumin supplementation failed to attenuate insulitis in NOD mice. CONCLUSIONS: These data provide evidence that exercise training can mitigate T1D development in genetically susceptible mice. Springer International Publishing 2017-04-04 /pmc/articles/PMC5380567/ /pubmed/28378202 http://dx.doi.org/10.1186/s40798-017-0082-3 Text en © The Author(s). 2017 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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. |
spellingShingle | Original Research Article Oharomari, Leandro Kansuke de Moraes, Camila Navarro, Anderson Marliere Exercise Training but not Curcumin Supplementation Decreases Immune Cell Infiltration in the Pancreatic Islets of a Genetically Susceptible Model of Type 1 Diabetes |
title | Exercise Training but not Curcumin Supplementation Decreases Immune Cell Infiltration in the Pancreatic Islets of a Genetically Susceptible Model of Type 1 Diabetes |
title_full | Exercise Training but not Curcumin Supplementation Decreases Immune Cell Infiltration in the Pancreatic Islets of a Genetically Susceptible Model of Type 1 Diabetes |
title_fullStr | Exercise Training but not Curcumin Supplementation Decreases Immune Cell Infiltration in the Pancreatic Islets of a Genetically Susceptible Model of Type 1 Diabetes |
title_full_unstemmed | Exercise Training but not Curcumin Supplementation Decreases Immune Cell Infiltration in the Pancreatic Islets of a Genetically Susceptible Model of Type 1 Diabetes |
title_short | Exercise Training but not Curcumin Supplementation Decreases Immune Cell Infiltration in the Pancreatic Islets of a Genetically Susceptible Model of Type 1 Diabetes |
title_sort | exercise training but not curcumin supplementation decreases immune cell infiltration in the pancreatic islets of a genetically susceptible model of type 1 diabetes |
topic | Original Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5380567/ https://www.ncbi.nlm.nih.gov/pubmed/28378202 http://dx.doi.org/10.1186/s40798-017-0082-3 |
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