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Research Article | Open Access

Fucoidan dose-dependently alleviated hyperuricemia and modulated gut microbiota in mice

Yan-Xin Wang1,2,Xiao-Long Chen2,Kai Zhou4Lu-Lu Wang2Yu-Zhen Zhong2Jie Peng3Bao-Sheng Ge1Chi-Tang Ho3Chen-Yang Lu2( )
State Key Laboratory of Heavy Oil Processing and Center for Bioengineering and Biotechnology, China University of Petroleum (East China), Qingdao 266580, China
State Key Laboratory for Managing Biotic and Chemical Threats to the Quality and Safety of Agro-products and School of Marine Science, Ningbo University, Ningbo 315211, China
Department of Food Science, Rutgers University, New Brunswick, New Jersey 08901, USA
Ningbo Liwa Pharmaceutical Co., Ltd., Ningbo 315174, China

Yan-Xin Wang and Xiao-Long Chen contributed equally to this work.

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Highlights

(1) Fucoidan alleviated the phenotypes of hyperuricemia in a dose-dependent manner.

(2) Fucoidan inhibited the biosynthesis and reabsorption and promoted the excretion of uric acid.

(3) Fucoidan modulated gut microbiota along with the hyperuricemia alleviation.

Abstract

The global incidence of hyperuricemia (HUA) is gradually increasing, and HUA poses a severe threat to human health. Between 25% and 50% of HUA patients are not effectively treated with current clinical medications due to drug contraindications or severe adverse reactions. Therefore, novel safe and effective uric acid-lowering products are needed. Fucoidan is a naturally derived polysaccharide containing sulfate groups exclusively found in brown algae. Although there are reports on the anti-HUA effects of fucoidan, the simultaneous regulation of gut microbiota by anti-HUA still needs to be fully understood. In this study, potassium oxonate (PO) and hypoxanthine-induced HUA model mice were treated with 100, 200 and 400 mg/kg fucoidan (from Laminaria japonica) for 14 days. The levels associated with HUA were quantified using assay kits to assess fucoidan intervention. 16S rRNA gene sequencing was used to analyze the effects of fucoidan in mice with HUA. The results showed that fucoidan reduced serum uric acid and urea nitrogen levels in a dose-dependent manner, and serum creatinine levels in the 200 and 400 mg/kg fucoidan groups were similar to those in the control group. It decreased the expression of uric acid metabolic protein levels of xanthine oxidase (XOD), adenosine deaminase (ADA), and glucose transporter (GLUT9) and increased ATP binding cassette subfamily G member 2 (ABCG2) protein expression. 16S rRNA gene sequencing revealed that the richness (Chao and Ace indices) and diversity (Shannon and Simpson indices) of the gut microbiota in model mice decreased, whereas supplementation with fucoidan alleviated gut microbiota dysbiosis in HUA model mice, leading to a gradual approach of α-diversity and β-diversity towards the control mice. Additionally, fucoidan supplementation significantly increased the abundance of beneficial bacteria, which are negatively correlated with the HUA-associated phenotypes, reassuring the positive effects of fucoidan on gut health. This study proposed that fucoidan can be considered a potential candidate for preventing and treating HUA.

Graphical Abstract

Fucoidan (100, 200, and 400 mg/kg) alleviated the hyperuricemia (HUA) phenotype in a dose-dependent manner. Supplementation with fucoidan reduced the protein expression of uric acid-producing enzymes XOD and ADA, decreased the expression of the urate transporter GLUT9 involved in uric acid reabsorption, and increased the expression of the urate excretion transporter ABCG2. Additionally, fucoidan improved gut microbiota dysbiosis in HUA mice and significantly increased the abundance of beneficial bacteria negatively correlated with the HUA-related phenotype.

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Food & Medicine Homology
Article number: 9420095

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Cite this article:
Wang Y-X, Chen X-L, Zhou K, et al. Fucoidan dose-dependently alleviated hyperuricemia and modulated gut microbiota in mice. Food & Medicine Homology, 2026, 3(3): 9420095. https://doi.org/10.26599/FMH.2026.9420095

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Received: 18 August 2024
Revised: 10 September 2024
Accepted: 17 September 2024
Published: 12 March 2025
© National R & D Center for Edible Fungus Processing Technology 2025. Published by Tsinghua University Press.

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).