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.

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; I Wolf, Federica. - In: NUTRIENTS. - ISSN 2072-6643. - 13:12(2021). [10.3390/nu13124188]

Dietary magnesium alleviates experimental murine colitis through modulation of gut microbiota

Giuseppe Pietropaolo;
2021

Abstract

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.
2021
bifidobacterium; enterobacteriacee; dextran sodium sulfate; dysbiosis; inflammatory bowel disease; magnesemia; magnesium supplementation; metabolism
01 Pubblicazione su rivista::01a Articolo in rivista
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; I Wolf, Federica. - In: NUTRIENTS. - ISSN 2072-6643. - 13:12(2021). [10.3390/nu13124188]
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/1603155
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