Article(id=1315696209239585520, tenantId=1146029695717560320, journalId=1315121759093096577, issueId=1315696195121558078, articleNumber=null, orderNo=null, doi=10.3969/j.issn.1005-7021.2026.04.010, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1765123200000, receivedDateStr=2025-12-08, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1791616020736, onlineDateStr=2026-10-10, pubDate=1787155200000, pubDateStr=2026-08-20, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1791616020736, onlineIssueDateStr=2026-10-10, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1791616020736, creator=13701087609, updateTime=1791616020736, updator=13701087609, issue=Issue{id=1315696195121558078, tenantId=1146029695717560320, journalId=1315121759093096577, year='2026', volume='46', issue='4', pageStart='1', pageEnd='144', issueExtLink='null', onlineDate='null', pubDate='1787155200000', pubDateStr='2026-08-20', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=1, specialIssue=null, createTime=1791616017369, creator='13701087609', updateTime=1791616161314, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1315696798950339227, tenantId=1146029695717560320, journalId=1315121759093096577, issueId=1315696195121558078, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1315696798950339228, tenantId=1146029695717560320, journalId=1315121759093096577, issueId=1315696195121558078, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=128, endPage=135, ext={EN=ArticleExt(id=1315696209428329201, articleId=1315696209239585520, tenantId=1146029695717560320, journalId=1315121759093096577, language=EN, title=Research Advances on the Relationship between Short-Chain Fatty Acids from the Gut Microbiota Metabolites and Hyperuricemia, columnId=null, journalTitle=Journal of Microbiology, columnName=null, runingTitle=null, highlight=null, articleAbstract=

Hyperuricemia, a disorder stemming from dysregulated uric acid metabolism, is characterized by elevated serum uric acid levels. Recent research has revealed a significant association between hyperuricemia and short-chain fatty acids (SCFAs:such as primarily acetate, propionate, and butyrate etc.) which are key metabolic products of gut microbiota derived from dietary fiber fermentation. These SCFAs exert multifaceted effects on host metabolism and immune responses through diverse mechanisms. It is critical importance to elucidate the pathophysiological mechanisms of SCFAs contributing to hyperuricemia, which might inform effective strategies by dietary interventions and pharmacological management for hyperuricemia. This review systematically summarizes the involvement of SCFAs in various physiological processes, including systemic inflammatory responses, and further discusses alterations in SCFA producing gut microbiota observed in hyperuricemia. Finally, the mechanisms of SCFAs alleviating hyperuricemia were explored, including the modulation of uric acid-associated proteins, enhancement of intestinal mucosal barrier function, and attenuation of inflammatory cascades. The review could offer novel perspectives on the interplay between SCFAs and hyperuricemia, and provide fresh insights into the clinical management and prevention for hyperuricemia.

, authors=Man-xi DU¹, Yi HE^{1, 4}, Yu-qiu ZHU¹, Wu-jin CHEN^{1, 3}, Yu-ping SUN^{1, 2, *}, authorsList=Man-xi DU, Yi HE, Yu-qiu ZHU, Wu-jin CHEN, Yu-ping SUN, authorCompany=null, correspAuthors=Yu-ping SUN, authorNote=null, correspAuthorsNote=null, copyrightStatement=null, copyrightOwner=null, extLink=null, articleAbsUrl=null, sourceXml=null, magXml=null, pdfUrl=null, pdf=null, pdfFileSize=null, pdfExtLink=null, richHtmlUrl=null, mobilePdfUrl=null, reviewReport=null, pdfFirstPage=null, abstractGraph=null, abstractGraphContent=null, abstractVideo=null, citation=null, cebUrl=null, magXmlContent=null, mapNumber=null, fund=null), CN=ArticleExt(id=1315696209671598834, articleId=1315696209239585520, tenantId=1146029695717560320, journalId=1315121759093096577, language=CN, title=肠道菌群代谢产物短链脂肪酸与高尿酸血症关系的研究进展, columnId=1315696198753825373, journalTitle=微生物学杂志, columnName=专题论述, runingTitle=null, highlight=null, articleAbstract=

高尿酸血症源于体内尿酸代谢的紊乱，是以血液中的尿酸水平升高为主要特性的一类疾病。研究表明，短链脂肪酸（SCFAs）（乙酸、丙酸、丁酸等）作为肠道菌群的代谢产物，与高尿酸血症的发生发展密切相关，其作为肠道菌群发酵膳食纤维的主要代谢产物，通过多种机制影响宿主的代谢与免疫反应。因此，明确SCFAs参与高尿酸血症病理生理机制，为高尿酸血症的饮食干预及药物治疗提供有效方案具有重要意义。本文系统归纳了SCFAs所参与的多种生理过程及涉及机体的炎症相关反应，总结了高尿酸血症产生SCFAs的肠道菌群丰度的变化，以及SCFAs通过调节尿酸相关蛋白、完善肠道黏膜屏障功能、减缓炎症反应等途径缓解高尿酸血症的机制，为理解SCFAs与高尿酸血症相互作用提供新的视角，还可为高尿酸血症的临床治疗及预防提供新策略。

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杜满茜　女，硕士研究生。研究方向为益生菌缓解高尿酸血症的机制。E-mail: 2544439768@qq.com

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杜满茜　女，硕士研究生。研究方向为益生菌缓解高尿酸血症的机制。E-mail: 2544439768@qq.com

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