@article{078aeac6cb224524b62c5bf5680517c2,
title = "Seaweed dietary fiber sodium alginate suppresses the migration of colonic inflammatory monocytes and diet-induced metabolic syndrome via the gut microbiota",
abstract = "Metabolic syndrome (MetS) is a multifactorial chronic metabolic disorder that affects ap-proximately 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 co-lonic inflammatory monocytes, which promote MetS development, in a gut microbiota-dependent manner. The abundance of Bacteroides was negatively correlated with that of inflammatory mono-cytes 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.",
keywords = "Gut microbiota, Inflammatory monocytes, Metabolic syndrome",
author = "Ryuta Ejima and Masahiro Akiyama and Hiroki Sato and Sawako Tomioka and Kyosuke Yakabe and Tatsuki Kimizuka and Natsumi Seki and Yumiko Fujimura and Akiyoshi Hirayama and Shinji Fukuda and Koji Hase and Kim, {Yun Gi}",
note = "Funding Information: Funding: This work was supported by research grants from the JSPS KAKENHI (JP17H05068 and JP20H03490 to Y.-G.K.), AMED (JP20gm1010009 to S.F.; JP18gm6010004h0003 to Y.-G.K.), JST ERATO (JPMJER1902 to S.F.), the Food Science Institute Foundation (to S.F.), Takeda Science Foundation (to S.F. and Y.-G.K.), the Naito Foundation (to Y.-G.K.), Yakult Bio-Science Foundation (to Y.-G.K.), and Mochida Memorial Foundation for Medical and Pharmaceutical Research (to Y.-G.K.). Funding Information: Conflicts of Interest: H.S. is an employee of Kaigen Pharma Co., Ltd., Osaka, Japan. This study was funded by Kaigen Pharma Co., Ltd. Funding Information: This work was supported by research grants from the JSPS KAKENHI (JP17H05068 and JP20H03490 to Y.-G.K.), AMED (JP20gm1010009 to S.F.; JP18gm6010004h0003 to Y.-G.K.), JST ER-ATO (JPMJER1902 to S.F.), the Food Science Institute Foundation (to S.F.), Takeda Science Foundation (to S.F. and Y.-G.K.), the Naito Foundation (to Y.-G.K.), Yakult Bio-Science Foundation (to Y.-G.K.), and Mochida Memorial Foundation for Medical and Pharmaceutical Research (to Y.-G.K.). We would like to thank Ikuo Kimura, Junki Miyamoto, and Daisuke Takahashi for the technical help and Naofumi Mukaida for providing Ccr2?/? mice. We would also like to acknowledge the Animal Facility at the Keio University Faculty of Pharmacy for the breeding and maintenance of our mouse strains and the Instrument Management Division. We are grateful to editage (https://www.editage.jp, accessed on 28 July 2021) for editing a draft of this manuscript. Graphical abstract was created using www.biorender.io (accessed on 27 July 2021). Publisher Copyright: {\textcopyright} 2021 by the authors. Li-censee MDPI, Basel, Switzerland.",
year = "2021",
month = aug,
doi = "10.3390/nu13082812",
language = "English",
volume = "13",
journal = "Nutrients",
issn = "2072-6643",
publisher = "Multidisciplinary Digital Publishing Institute (MDPI)",
number = "8",
}