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Diet, Microbiota and Immune System in Type 1 Diabetes Development and Evolution

Type 1 diabetes (T1D) is the second most frequent autoimmune disease in childhood. The long-term micro- and macro-vascular complications of diabetes are associated with the leading causes of disability and even mortality in young adults. Understanding the T1D etiology will allow the design of preven...

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Autores principales: Mejía-León, María E., Calderón de la Barca, Ana M.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4663589/
https://www.ncbi.nlm.nih.gov/pubmed/26561831
http://dx.doi.org/10.3390/nu7115461
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author Mejía-León, María E.
Calderón de la Barca, Ana M.
author_facet Mejía-León, María E.
Calderón de la Barca, Ana M.
author_sort Mejía-León, María E.
collection PubMed
description Type 1 diabetes (T1D) is the second most frequent autoimmune disease in childhood. The long-term micro- and macro-vascular complications of diabetes are associated with the leading causes of disability and even mortality in young adults. Understanding the T1D etiology will allow the design of preventive strategies to avoid or delay the T1D onset and to help to maintain control after developing. T1D development involves genetic and environmental factors, such as birth delivery mode, use of antibiotics, and diet. Gut microbiota could be the link between environmental factors, the development of autoimmunity, and T1D. In this review, we will focus on the dietary factor and its relationship with the gut microbiota in the complex process involved in autoimmunity and T1D. The molecular mechanisms involved will also be addressed, and finally, evidence-based strategies for potential primary and secondary prevention of T1D will be discussed.
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spelling pubmed-46635892015-12-10 Diet, Microbiota and Immune System in Type 1 Diabetes Development and Evolution Mejía-León, María E. Calderón de la Barca, Ana M. Nutrients Review Type 1 diabetes (T1D) is the second most frequent autoimmune disease in childhood. The long-term micro- and macro-vascular complications of diabetes are associated with the leading causes of disability and even mortality in young adults. Understanding the T1D etiology will allow the design of preventive strategies to avoid or delay the T1D onset and to help to maintain control after developing. T1D development involves genetic and environmental factors, such as birth delivery mode, use of antibiotics, and diet. Gut microbiota could be the link between environmental factors, the development of autoimmunity, and T1D. In this review, we will focus on the dietary factor and its relationship with the gut microbiota in the complex process involved in autoimmunity and T1D. The molecular mechanisms involved will also be addressed, and finally, evidence-based strategies for potential primary and secondary prevention of T1D will be discussed. MDPI 2015-11-06 /pmc/articles/PMC4663589/ /pubmed/26561831 http://dx.doi.org/10.3390/nu7115461 Text en © 2015 by the authors; licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons by Attribution (CC-BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Mejía-León, María E.
Calderón de la Barca, Ana M.
Diet, Microbiota and Immune System in Type 1 Diabetes Development and Evolution
title Diet, Microbiota and Immune System in Type 1 Diabetes Development and Evolution
title_full Diet, Microbiota and Immune System in Type 1 Diabetes Development and Evolution
title_fullStr Diet, Microbiota and Immune System in Type 1 Diabetes Development and Evolution
title_full_unstemmed Diet, Microbiota and Immune System in Type 1 Diabetes Development and Evolution
title_short Diet, Microbiota and Immune System in Type 1 Diabetes Development and Evolution
title_sort diet, microbiota and immune system in type 1 diabetes development and evolution
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4663589/
https://www.ncbi.nlm.nih.gov/pubmed/26561831
http://dx.doi.org/10.3390/nu7115461
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