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...

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Bibliographic Details
Published in:Nutrients 2021-08, Vol.13 (8), p.2812
Main Authors: 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
Format: Article
Language:English
Subjects:
Abundance
Algae
Alginic acid
Antibiotics
Antibodies
Bacteroides
Biotechnology industry
Body weight
Body weight gain
Cellulose
Cholesterol
Composition
Diet
Dietary fiber
Ethylenediaminetetraacetic acid
Euthanasia
Feces
Fiber in human nutrition
Flow cytometry
Glucose
Glucose tolerance
gut microbiota
High fat diet
Inflammation
inflammatory monocytes
Insulin resistance
Intestinal microflora
Lipids
Metabolic disorders
Metabolic syndrome
Metabolites
Microbiota
Microbiota (Symbiotic organisms)
Monocytes
Novel foods
Obesity
Seaweeds
Sodium
Sodium alginate
Type 2 diabetes
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Summary: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.
ISSN:2072-6643
2072-6643
DOI:10.3390/nu13082812