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Use of Ghrelin as a Treatment for Inflammatory Bowel Disease: Mechanistic Considerations

Inflammatory bowel diseases (IBD)—and in particular Crohn's disease—are immune-mediated processes that result in denuded intestinal mucosa and can produce decreased appetite, weight loss, and systemic inflammation. Current treatments include anti-inflammatory medications, immunomodulators, and...

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Autor principal: DeBoer, Mark D.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3154487/
https://www.ncbi.nlm.nih.gov/pubmed/21845198
http://dx.doi.org/10.1155/2011/189242
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author DeBoer, Mark D.
author_facet DeBoer, Mark D.
author_sort DeBoer, Mark D.
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description Inflammatory bowel diseases (IBD)—and in particular Crohn's disease—are immune-mediated processes that result in denuded intestinal mucosa and can produce decreased appetite, weight loss, and systemic inflammation. Current treatments include anti-inflammatory medications, immunomodulators, and feeding interventions. Ghrelin is an endogenous orexigenic hormone that directly stimulates growth hormone release, increases gut motility, and has cardiovascular and anti-inflammatory properties. Although ghrelin levels are elevated in active IBD, administration of ghrelin in most (but not all) animal models of colitis has produced improvements in disease activity and systemic inflammation. The mechanism for these effects is not known but may relate to decreased inflammation, increased motility, increased appetite, and increased colonic blood flow. Human trials have not been performed, however, and more research is clearly needed.
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spelling pubmed-31544872011-08-15 Use of Ghrelin as a Treatment for Inflammatory Bowel Disease: Mechanistic Considerations DeBoer, Mark D. Int J Pept Review Article Inflammatory bowel diseases (IBD)—and in particular Crohn's disease—are immune-mediated processes that result in denuded intestinal mucosa and can produce decreased appetite, weight loss, and systemic inflammation. Current treatments include anti-inflammatory medications, immunomodulators, and feeding interventions. Ghrelin is an endogenous orexigenic hormone that directly stimulates growth hormone release, increases gut motility, and has cardiovascular and anti-inflammatory properties. Although ghrelin levels are elevated in active IBD, administration of ghrelin in most (but not all) animal models of colitis has produced improvements in disease activity and systemic inflammation. The mechanism for these effects is not known but may relate to decreased inflammation, increased motility, increased appetite, and increased colonic blood flow. Human trials have not been performed, however, and more research is clearly needed. Hindawi Publishing Corporation 2011 2011-08-09 /pmc/articles/PMC3154487/ /pubmed/21845198 http://dx.doi.org/10.1155/2011/189242 Text en Copyright © 2011 Mark D. DeBoer. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
DeBoer, Mark D.
Use of Ghrelin as a Treatment for Inflammatory Bowel Disease: Mechanistic Considerations
title Use of Ghrelin as a Treatment for Inflammatory Bowel Disease: Mechanistic Considerations
title_full Use of Ghrelin as a Treatment for Inflammatory Bowel Disease: Mechanistic Considerations
title_fullStr Use of Ghrelin as a Treatment for Inflammatory Bowel Disease: Mechanistic Considerations
title_full_unstemmed Use of Ghrelin as a Treatment for Inflammatory Bowel Disease: Mechanistic Considerations
title_short Use of Ghrelin as a Treatment for Inflammatory Bowel Disease: Mechanistic Considerations
title_sort use of ghrelin as a treatment for inflammatory bowel disease: mechanistic considerations
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3154487/
https://www.ncbi.nlm.nih.gov/pubmed/21845198
http://dx.doi.org/10.1155/2011/189242
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