Article(id=1226136787546976641, tenantId=1146029695717560320, journalId=1192105938417971205, issueId=1226136782408954119, articleNumber=null, orderNo=null, doi=10.13343/j.cnki.wsxb.20250639, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=research-article, receivedDate=1755532800000, receivedDateStr=2025-08-19, revisedDate=null, revisedDateStr=null, acceptedDate=1760112000000, acceptedDateStr=2025-10-11, onlineDate=1770263390671, onlineDateStr=2026-02-05, pubDate=1770134400000, pubDateStr=2026-02-04, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1770263390671, onlineIssueDateStr=2026-02-05, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1770263390671, creator=13701087609, updateTime=1770263390671, updator=13701087609, issue=Issue{id=1226136782408954119, tenantId=1146029695717560320, journalId=1192105938417971205, year='2026', volume='66', issue='2', pageStart='481', pageEnd='955', issueExtLink='null', onlineDate='null', pubDate='null', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1770263389446, creator=13701087609, updateTime=1770268138976, updator=13701087609, preIssue=null, nextIssue=null, ext={EN=IssueExt(id=1226156703490683529, tenantId=1146029695717560320, journalId=1192105938417971205, issueId=1226136782408954119, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1226156703490683530, tenantId=1146029695717560320, journalId=1192105938417971205, issueId=1226136782408954119, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null}, startPage=547, endPage=559, ext={EN=ArticleExt(id=1226136789082091940, articleId=1226136787546976641, tenantId=1146029695717560320, journalId=1192105938417971205, language=EN, title=Research progress in the amelioration of hyperuricemia by gut microbiota, columnId=1192149543727808575, journalTitle=Acta Microbiologica Sinica, columnName=Review, runingTitle=null, highlight=null, articleAbstract=

Hyperuricemia is a pathological phenomenon in which the metabolism of uric acid in the human body is disrupted and blood uric acid levels remain above normal. In recent years, gut microbiota has become a research hotspot for various metabolic diseases, serving as a potential new target for the prevention and treatment of hyperuricemia. This article reviews the metabolic pathways and physiological effects of uric acid in the human body and elucidates the regulatory mechanisms of gut microbiota on hyperuricemia. Such mechanisms include inhibiting uric acid synthesis by the breakdown and internalization of purines, degrading uric acid and promoting uric acid excretion, repairing intestinal barriers, influencing intestinal metabolites, and regulating intestinal immunity. In addition, this article summarizes the potential applications of optimizing dietary structure, taking probiotics and prebiotics, and fecal microbiota transplantation in the treatment of hyperuricemia, providing new ideas and references for the prevention and treatment of hyperuricemia.

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高尿酸血症(hyperuricemia, HUA)是人体内尿酸代谢紊乱、血尿酸水平持续高于正常值的一种病理现象。近年来，肠道微生态成为各种代谢性疾病的研究热点，因此肠道菌群有可能成为预防和治疗高尿酸血症的新靶标。本文综述了尿酸在人体内的代谢途径和生理作用，阐述了肠道菌群对高尿酸血症的调控机制，包括分解与内化嘌呤以抑制尿酸合成、分解尿酸并促进尿酸排泄、修复肠道屏障、影响肠道代谢产物、调节肠道免疫等方面。同时，总结了优化饮食结构、服用益生菌、益生元干预及粪便微生物移植等方法在高尿酸血症治疗中的潜在应用，为高尿酸血症的防治提供了新的思路与参考。

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Association of dietary patterns with serum uric acid and hyperuricemia in Chinese adults[J]. Chinese Journal of Epidemiology, 2024, 45(10): 1403-1409 (in Chinese)., articleTitle=null, refAbstract=null)], funds=[Fund(id=1226195550614241318, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1226136787546976641, awardId=RJTJ25-MS-060, language=EN, fundingSource=the Youth Promotion Program of the Peak Climbing Plan for Discipline Construction of Renji Hospital Affiliated to Shanghai Jiao Tong University School of Medicine—“Challenge and Acceptance” Series Projects(RJTJ25-MS-060), fundOrder=null, country=null), Fund(id=1226195550773624879, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1226136787546976641, awardId=RJTJ25-MS-060, language=CN, fundingSource=上海交通大学医学院附属仁济医院学科建设攀峰计划—“揭榜挂帅”系列项目面青推进类项目(RJTJ25-MS-060), fundOrder=null, country=null), Fund(id=1226195550895259704, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1226136787546976641, awardId=202401AT070846, language=EN, fundingSource=the Basic Research Project of Yunnan Provincial Department of Science and Technology(202401AT070846), fundOrder=null, country=null), Fund(id=1226195551004311614, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1226136787546976641, awardId=202401AT070846, language=CN, fundingSource=云南省科技厅基础研究专项(202401AT070846), fundOrder=null, country=null)], companyList=[AuthorCompany(id=1226195546344440598, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1226136787546976641, xref=1., ext=[AuthorCompanyExt(id=1226195546352829207, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1226136787546976641, companyId=1226195546344440598, language=EN, country=null, province=null, city=null, postcode=null, companyName=null, departmentName=null, remark=^1.Faculty of Life Science and Technology, Kunming University of Science and Technology, Kunming, Yunnan, China), AuthorCompanyExt(id=1226195546357023513, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1226136787546976641, companyId=1226195546344440598, language=CN, country=null, province=null, city=null, postcode=null, companyName=null, departmentName=null, remark=^1.昆明理工大学 生命科学与技术学院，云南 昆明)]), AuthorCompany(id=1226195546432520989, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1226136787546976641, xref=2., ext=[AuthorCompanyExt(id=1226195546436715293, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1226136787546976641, companyId=1226195546432520989, language=EN, country=null, province=null, city=null, postcode=null, companyName=null, departmentName=null, remark=^2.Department of Endocrinology and Metabolism, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China), AuthorCompanyExt(id=1226195546445103902, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1226136787546976641, companyId=1226195546432520989, language=CN, country=null, province=null, city=null, postcode=null, companyName=null, departmentName=null, remark=^2.上海交通大学医学院附属仁济医院内分泌科，上海)])], figs=[ArticleFig(id=1226195548630336480, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1226136787546976641, language=EN, label=Figure 1, caption=Pathogenesis of hyperuricemia. Blood uric acid levels are regulated by the dynamic balance of uric acid formation and excretion. When uric acid synthesis is excessive, excretion is impaired, or both, the blood uric acid level rises, which in turn induces HUA., figureFileSmall=vy/EEopQpCqP4114/hUbbQ==, figureFileBig=jGKwjpdOjSuZ+L8RYpYCyg==, tableContent=null), ArticleFig(id=1226195548705833963, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1226136787546976641, language=CN, label=图1, caption=高尿酸血症发病机制。血尿酸水平受尿酸形成和排泄的动态平衡调控。当尿酸合成过多、排泄障碍或两者兼有时血尿酸水平升高，进而诱发HUA。, figureFileSmall=vy/EEopQpCqP4114/hUbbQ==, figureFileBig=jGKwjpdOjSuZ+L8RYpYCyg==, tableContent=null), ArticleFig(id=1226195548823274486, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1226136787546976641, language=EN, label=Figure 2, caption=The regulatory mechanism of gut microbiota on hyperuricemia. The gut microbiota can alleviate hyperuricemia through multiple pathways, mainly by decomposing and internalizing purines to inhibit uric acid synthesis, decomposing uric acid, and promoting uric acid excretion, as well as regulating the intestinal barrier., figureFileSmall=lYauHbJZnppa+kV4PPmO9Q==, figureFileBig=mlCTvgEomIlLokgOOFg+3g==, tableContent=null), ArticleFig(id=1226195550161256449, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1226136787546976641, language=CN, label=图2, caption=肠道微生物对高尿酸血症的调控机制。肠道菌群可多途径缓解高尿酸血症，其作用机制主要包括分解和内化嘌呤抑制尿酸合成、分解尿酸和促进尿酸排泄，以及调节肠道屏障。, figureFileSmall=lYauHbJZnppa+kV4PPmO9Q==, figureFileBig=mlCTvgEomIlLokgOOFg+3g==, tableContent=null), ArticleFig(id=1226195550257725448, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1226136787546976641, language=EN, label=Table 1, caption=

HUA intervention measures based on gut microbiota

, figureFileSmall=null, figureFileBig=null, tableContent=

Intervention	Specific measures	Mechanism of action	References
Dietary structure adjustment	DASH diet The mediterranean diet Low purine diet Ketogenic diet	Reduce exogenous purine intake Promote SCFAs production inhibit uric acid synthase (XOD) Competitive inhibition of renal tubular uric acid reabsorption by whey protein Polyphenolic substances inhibit inflammation and XOD activity	[80]
Probiotic intervention	Bifidobacterium adolescentis Lactobacillus acidophilus Lactiplantibacillus plantarum Lacticaseibacillus rhamnosus	Direct degradation of intestinal purine/uric acid Strengthening the intestinal barrier and reducing the entry of endotoxins into the bloodstream Inhibition of xanthine oxidase (XOD) activity Regulating Th17/Treg immune balance to alleviate inflammation	[81]
Probiotic supplementation	Soluble fiber: oligofructose (FOS), inulin Resistant starch: green banana, cold rice Polyphenols: green tea extract, berries	Selective promotion of probiotic (Bifidobacterium/Lactobacillus) proliferation Fermentation produces SCFAs such as butyric acid, which downregulate the URAT1 transporter protein Antioxidant effect reduces systemic inflammation	[82]
Fecal microbiota transplantation	Screening of healthy donor microbiota (characteristics of low uric acid type microbiota) Delivery via colonoscopy/capsule	Rebuilding gut microbiota structure: increasing uric acid degrading bacteria (such as Bacillus subtilis), reducing pro-inflammatory bacteria (such as Prevotella), restoring intestinal barrier integrity	[83]

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基于肠道微生物的HUA干预措施

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Intervention	Specific measures	Mechanism of action	References
Dietary structure adjustment	DASH diet The mediterranean diet Low purine diet Ketogenic diet	Reduce exogenous purine intake Promote SCFAs production inhibit uric acid synthase (XOD) Competitive inhibition of renal tubular uric acid reabsorption by whey protein Polyphenolic substances inhibit inflammation and XOD activity	[80]
Probiotic intervention	Bifidobacterium adolescentis Lactobacillus acidophilus Lactiplantibacillus plantarum Lacticaseibacillus rhamnosus	Direct degradation of intestinal purine/uric acid Strengthening the intestinal barrier and reducing the entry of endotoxins into the bloodstream Inhibition of xanthine oxidase (XOD) activity Regulating Th17/Treg immune balance to alleviate inflammation	[81]
Probiotic supplementation	Soluble fiber: oligofructose (FOS), inulin Resistant starch: green banana, cold rice Polyphenols: green tea extract, berries	Selective promotion of probiotic (Bifidobacterium/Lactobacillus) proliferation Fermentation produces SCFAs such as butyric acid, which downregulate the URAT1 transporter protein Antioxidant effect reduces systemic inflammation	[82]
Fecal microbiota transplantation	Screening of healthy donor microbiota (characteristics of low uric acid type microbiota) Delivery via colonoscopy/capsule	Rebuilding gut microbiota structure: increasing uric acid degrading bacteria (such as Bacillus subtilis), reducing pro-inflammatory bacteria (such as Prevotella), restoring intestinal barrier integrity	[83]

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