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Gut microbiota and sirtuins in obesity-related inflammation and bowel dysfunction

Obesity is a chronic disease characterized by persistent low-grade inflammation with alterations in gut motility. Motor abnormalities suggest that obesity has effects on the enteric nervous system (ENS), which controls virtually all gut functions. Recent studies have revealed that the gut microbiota...

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Detalles Bibliográficos
Autores principales: Lakhan, Shaheen E, Kirchgessner, Annette
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3235071/
https://www.ncbi.nlm.nih.gov/pubmed/22115311
http://dx.doi.org/10.1186/1479-5876-9-202
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author Lakhan, Shaheen E
Kirchgessner, Annette
author_facet Lakhan, Shaheen E
Kirchgessner, Annette
author_sort Lakhan, Shaheen E
collection PubMed
description Obesity is a chronic disease characterized by persistent low-grade inflammation with alterations in gut motility. Motor abnormalities suggest that obesity has effects on the enteric nervous system (ENS), which controls virtually all gut functions. Recent studies have revealed that the gut microbiota can affect obesity and increase inflammatory tone by modulating mucosal barrier function. Furthermore, the observation that inflammatory conditions influence the excitability of enteric neurons may add to the gut dysfunction in obesity. In this article, we discuss recent advances in understanding the role of gut microbiota and inflammation in the pathogenesis of obesity and obesity-related gastrointestinal dysfunction. The potential contribution of sirtuins in protecting or regulating the circuitry of the ENS under inflamed states is also considered.
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spelling pubmed-32350712011-12-10 Gut microbiota and sirtuins in obesity-related inflammation and bowel dysfunction Lakhan, Shaheen E Kirchgessner, Annette J Transl Med Review Obesity is a chronic disease characterized by persistent low-grade inflammation with alterations in gut motility. Motor abnormalities suggest that obesity has effects on the enteric nervous system (ENS), which controls virtually all gut functions. Recent studies have revealed that the gut microbiota can affect obesity and increase inflammatory tone by modulating mucosal barrier function. Furthermore, the observation that inflammatory conditions influence the excitability of enteric neurons may add to the gut dysfunction in obesity. In this article, we discuss recent advances in understanding the role of gut microbiota and inflammation in the pathogenesis of obesity and obesity-related gastrointestinal dysfunction. The potential contribution of sirtuins in protecting or regulating the circuitry of the ENS under inflamed states is also considered. BioMed Central 2011-11-24 /pmc/articles/PMC3235071/ /pubmed/22115311 http://dx.doi.org/10.1186/1479-5876-9-202 Text en Copyright ©2011 Lakhan and Kirchgessner; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review
Lakhan, Shaheen E
Kirchgessner, Annette
Gut microbiota and sirtuins in obesity-related inflammation and bowel dysfunction
title Gut microbiota and sirtuins in obesity-related inflammation and bowel dysfunction
title_full Gut microbiota and sirtuins in obesity-related inflammation and bowel dysfunction
title_fullStr Gut microbiota and sirtuins in obesity-related inflammation and bowel dysfunction
title_full_unstemmed Gut microbiota and sirtuins in obesity-related inflammation and bowel dysfunction
title_short Gut microbiota and sirtuins in obesity-related inflammation and bowel dysfunction
title_sort gut microbiota and sirtuins in obesity-related inflammation and bowel dysfunction
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3235071/
https://www.ncbi.nlm.nih.gov/pubmed/22115311
http://dx.doi.org/10.1186/1479-5876-9-202
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