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Seaweed Dietary Fiber Sodium Alginate Suppresses the Migration of Colonic Inflammatory Monocytes and Diet-Induced Metabolic Syndrome via the Gut Microbiota
Metabolic syndrome (MetS) is a multifactorial chronic metabolic disorder that affects approximately one billion people worldwide. Recent studies have evaluated whether targeting the gut microbiota can prevent MetS. This study aimed to assess the ability of dietary fiber to control MetS by modulating...
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/PMC8401899/ https://www.ncbi.nlm.nih.gov/pubmed/34444972 http://dx.doi.org/10.3390/nu13082812 |
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author | Ejima, Ryuta Akiyama, Masahiro Sato, Hiroki Tomioka, Sawako Yakabe, Kyosuke Kimizuka, Tatsuki Seki, Natsumi Fujimura, Yumiko Hirayama, Akiyoshi Fukuda, Shinji Hase, Koji Kim, Yun-Gi |
author_facet | Ejima, Ryuta Akiyama, Masahiro Sato, Hiroki Tomioka, Sawako Yakabe, Kyosuke Kimizuka, Tatsuki Seki, Natsumi Fujimura, Yumiko Hirayama, Akiyoshi Fukuda, Shinji Hase, Koji Kim, Yun-Gi |
author_sort | Ejima, Ryuta |
collection | PubMed |
description | Metabolic syndrome (MetS) is a multifactorial chronic metabolic disorder that affects approximately one billion people worldwide. Recent studies have evaluated whether targeting the gut microbiota can prevent MetS. This study aimed to assess the ability of dietary fiber to control MetS by modulating gut microbiota composition. Sodium alginate (SA) is a seaweed-derived dietary fiber that suppresses high-fat diet (HFD)-induced MetS via an effect on the gut microbiota. We observed that SA supplementation significantly decreased body weight gain, cholesterol levels, and fat weight, while improving glucose tolerance in HFD-fed mice. SA changed the gut microbiota composition and significantly increased the abundance of Bacteroides. Antibiotic treatment completely abolished the suppressive effects of SA on MetS. Mechanistically, SA decreased the number of colonic inflammatory monocytes, which promote MetS development, in a gut microbiota-dependent manner. The abundance of Bacteroides was negatively correlated with that of inflammatory monocytes and positively correlated with the levels of several gut metabolites. The present study revealed a novel food function of SA in preventing HFD-induced MetS through its action on gut microbiota. |
format | Online Article Text |
id | pubmed-8401899 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-84018992021-08-29 Seaweed Dietary Fiber Sodium Alginate Suppresses the Migration of Colonic Inflammatory Monocytes and Diet-Induced Metabolic Syndrome via the Gut Microbiota Ejima, Ryuta Akiyama, Masahiro Sato, Hiroki Tomioka, Sawako Yakabe, Kyosuke Kimizuka, Tatsuki Seki, Natsumi Fujimura, Yumiko Hirayama, Akiyoshi Fukuda, Shinji Hase, Koji Kim, Yun-Gi Nutrients Article Metabolic syndrome (MetS) is a multifactorial chronic metabolic disorder that affects approximately one billion people worldwide. Recent studies have evaluated whether targeting the gut microbiota can prevent MetS. This study aimed to assess the ability of dietary fiber to control MetS by modulating gut microbiota composition. Sodium alginate (SA) is a seaweed-derived dietary fiber that suppresses high-fat diet (HFD)-induced MetS via an effect on the gut microbiota. We observed that SA supplementation significantly decreased body weight gain, cholesterol levels, and fat weight, while improving glucose tolerance in HFD-fed mice. SA changed the gut microbiota composition and significantly increased the abundance of Bacteroides. Antibiotic treatment completely abolished the suppressive effects of SA on MetS. Mechanistically, SA decreased the number of colonic inflammatory monocytes, which promote MetS development, in a gut microbiota-dependent manner. The abundance of Bacteroides was negatively correlated with that of inflammatory monocytes and positively correlated with the levels of several gut metabolites. The present study revealed a novel food function of SA in preventing HFD-induced MetS through its action on gut microbiota. MDPI 2021-08-16 /pmc/articles/PMC8401899/ /pubmed/34444972 http://dx.doi.org/10.3390/nu13082812 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 Ejima, Ryuta Akiyama, Masahiro Sato, Hiroki Tomioka, Sawako Yakabe, Kyosuke Kimizuka, Tatsuki Seki, Natsumi Fujimura, Yumiko Hirayama, Akiyoshi Fukuda, Shinji Hase, Koji Kim, Yun-Gi Seaweed Dietary Fiber Sodium Alginate Suppresses the Migration of Colonic Inflammatory Monocytes and Diet-Induced Metabolic Syndrome via the Gut Microbiota |
title | Seaweed Dietary Fiber Sodium Alginate Suppresses the Migration of Colonic Inflammatory Monocytes and Diet-Induced Metabolic Syndrome via the Gut Microbiota |
title_full | Seaweed Dietary Fiber Sodium Alginate Suppresses the Migration of Colonic Inflammatory Monocytes and Diet-Induced Metabolic Syndrome via the Gut Microbiota |
title_fullStr | Seaweed Dietary Fiber Sodium Alginate Suppresses the Migration of Colonic Inflammatory Monocytes and Diet-Induced Metabolic Syndrome via the Gut Microbiota |
title_full_unstemmed | Seaweed Dietary Fiber Sodium Alginate Suppresses the Migration of Colonic Inflammatory Monocytes and Diet-Induced Metabolic Syndrome via the Gut Microbiota |
title_short | Seaweed Dietary Fiber Sodium Alginate Suppresses the Migration of Colonic Inflammatory Monocytes and Diet-Induced Metabolic Syndrome via the Gut Microbiota |
title_sort | seaweed dietary fiber sodium alginate suppresses the migration of colonic inflammatory monocytes and diet-induced metabolic syndrome via the gut microbiota |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8401899/ https://www.ncbi.nlm.nih.gov/pubmed/34444972 http://dx.doi.org/10.3390/nu13082812 |
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