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Dietary Magnesium Alleviates Experimental Murine Colitis through Modulation of Gut Microbiota
Nutritional deficiencies are common in inflammatory bowel diseases (IBD). In patients, magnesium (Mg) deficiency is associated with disease severity, while in murine models, dietary Mg supplementation contributes to restoring mucosal function. Since Mg availability modulates key bacterial functions,...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8707433/ https://www.ncbi.nlm.nih.gov/pubmed/34959740 http://dx.doi.org/10.3390/nu13124188 |
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author | Del Chierico, Federica Trapani, Valentina Petito, Valentina Reddel, Sofia Pietropaolo, Giuseppe Graziani, Cristina Masi, Letizia Gasbarrini, Antonio Putignani, Lorenza Scaldaferri, Franco Wolf, Federica I. |
author_facet | Del Chierico, Federica Trapani, Valentina Petito, Valentina Reddel, Sofia Pietropaolo, Giuseppe Graziani, Cristina Masi, Letizia Gasbarrini, Antonio Putignani, Lorenza Scaldaferri, Franco Wolf, Federica I. |
author_sort | Del Chierico, Federica |
collection | PubMed |
description | Nutritional deficiencies are common in inflammatory bowel diseases (IBD). In patients, magnesium (Mg) deficiency is associated with disease severity, while in murine models, dietary Mg supplementation contributes to restoring mucosal function. Since Mg availability modulates key bacterial functions, including growth and virulence, we investigated whether the beneficial effects of Mg supplementation during colitis might be mediated by gut microbiota. The effects of dietary Mg modulation were assessed in a murine model of dextran sodium sulfate (DSS)-induced colitis by monitoring magnesemia, weight, and fecal consistency. Gut microbiota were analyzed by 16S-rRNA based profiling on fecal samples. Mg supplementation improved microbiota richness in colitic mice, increased abundance of Bifidobacterium and reduced Enterobacteriaceae. KEEG pathway analysis predicted an increase in biosynthetic metabolism, DNA repair and translation pathways during Mg supplementation and in the presence of colitis, while low Mg conditions favored catabolic processes. Thus, dietary Mg supplementation increases bacteria involved in intestinal health and metabolic homeostasis, and reduces bacteria involved in inflammation and associated with human diseases, such as IBD. These findings suggest that Mg supplementation may be a safe and cost-effective strategy to ameliorate disease symptoms and restore a beneficial intestinal flora in IBD patients. |
format | Online Article Text |
id | pubmed-8707433 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-87074332021-12-25 Dietary Magnesium Alleviates Experimental Murine Colitis through Modulation of Gut Microbiota Del Chierico, Federica Trapani, Valentina Petito, Valentina Reddel, Sofia Pietropaolo, Giuseppe Graziani, Cristina Masi, Letizia Gasbarrini, Antonio Putignani, Lorenza Scaldaferri, Franco Wolf, Federica I. Nutrients Article Nutritional deficiencies are common in inflammatory bowel diseases (IBD). In patients, magnesium (Mg) deficiency is associated with disease severity, while in murine models, dietary Mg supplementation contributes to restoring mucosal function. Since Mg availability modulates key bacterial functions, including growth and virulence, we investigated whether the beneficial effects of Mg supplementation during colitis might be mediated by gut microbiota. The effects of dietary Mg modulation were assessed in a murine model of dextran sodium sulfate (DSS)-induced colitis by monitoring magnesemia, weight, and fecal consistency. Gut microbiota were analyzed by 16S-rRNA based profiling on fecal samples. Mg supplementation improved microbiota richness in colitic mice, increased abundance of Bifidobacterium and reduced Enterobacteriaceae. KEEG pathway analysis predicted an increase in biosynthetic metabolism, DNA repair and translation pathways during Mg supplementation and in the presence of colitis, while low Mg conditions favored catabolic processes. Thus, dietary Mg supplementation increases bacteria involved in intestinal health and metabolic homeostasis, and reduces bacteria involved in inflammation and associated with human diseases, such as IBD. These findings suggest that Mg supplementation may be a safe and cost-effective strategy to ameliorate disease symptoms and restore a beneficial intestinal flora in IBD patients. MDPI 2021-11-23 /pmc/articles/PMC8707433/ /pubmed/34959740 http://dx.doi.org/10.3390/nu13124188 Text en © 2021 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Del Chierico, Federica Trapani, Valentina Petito, Valentina Reddel, Sofia Pietropaolo, Giuseppe Graziani, Cristina Masi, Letizia Gasbarrini, Antonio Putignani, Lorenza Scaldaferri, Franco Wolf, Federica I. Dietary Magnesium Alleviates Experimental Murine Colitis through Modulation of Gut Microbiota |
title | Dietary Magnesium Alleviates Experimental Murine Colitis through Modulation of Gut Microbiota |
title_full | Dietary Magnesium Alleviates Experimental Murine Colitis through Modulation of Gut Microbiota |
title_fullStr | Dietary Magnesium Alleviates Experimental Murine Colitis through Modulation of Gut Microbiota |
title_full_unstemmed | Dietary Magnesium Alleviates Experimental Murine Colitis through Modulation of Gut Microbiota |
title_short | Dietary Magnesium Alleviates Experimental Murine Colitis through Modulation of Gut Microbiota |
title_sort | dietary magnesium alleviates experimental murine colitis through modulation of gut microbiota |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8707433/ https://www.ncbi.nlm.nih.gov/pubmed/34959740 http://dx.doi.org/10.3390/nu13124188 |
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