<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Zhao H</submitter><funding>Science and Technology Planning Project of Chengguan District, Lanzhou City</funding><funding>Hongliu Outstanding Youth program 2023</funding><funding>Key Research and Development Program of Gannan Prefecture</funding><funding>National Natural Science Foundation of China</funding><pagination>409</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12896772</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>15(3)</volume><pubmed_abstract>Fructose dietary intake is one of the most common risk factors for hyperuricemia, which is a critical threat to human health, and the lack of an effective biological intervention method is the main problem in preventing hyperuricemia caused by fructose intake. &lt;i>Lacticaseibacillus rhamnosus&lt;/i> Fmb14 (&lt;i>L. rhamnosus&lt;/i> Fmb14) has a fructose-metabolizing ability to produce extracellular polysaccharides (EPSs), and the yield of EPSs reached 0.50 and 0.42 g/L after 48 h of fermentation in liquid media of glucose-MRS and fructose-MRS. Six pure polysaccharide components were obtained after purification. A hyperuricemic mouse model was subsequently established by feeding a 60% high-fructose diet with potassium oxyazinate for 8 weeks, and the results revealed that &lt;i>L. rhamnosus&lt;/i> Fmb14 and</pubmed_abstract><journal>Foods (Basel, Switzerland)</journal><pubmed_title>Exopolysaccharides from &amp;lt;i&amp;gt;Lacticaseibacillus rhamnosus&amp;lt;/i&amp;gt; Fmb14 Ameliorate Fructose-Induced Hyperuricemia and Fatty Liver via Gut Modulation.</pubmed_title><pmcid>PMC12896772</pmcid><funding_grant_id>grants 2024RCCX0022 to Song Li</funding_grant_id><funding_grant_id>grants 2025ZY1N007 to Song Li</funding_grant_id><funding_grant_id>grants 062402 to Zhao Hongyuan</funding_grant_id><funding_grant_id>grants 32072182 to Zhaoxin Lu</funding_grant_id><pubmed_authors>Song L</pubmed_authors><pubmed_authors>Zhang Z</pubmed_authors><pubmed_authors>Lu Y</pubmed_authors><pubmed_authors>Lu Z</pubmed_authors><pubmed_authors>Tang C</pubmed_authors><pubmed_authors>Chen X</pubmed_authors><pubmed_authors>Zhao H</pubmed_authors></additional><is_claimable>false</is_claimable><name>Exopolysaccharides from &amp;lt;i&amp;gt;Lacticaseibacillus rhamnosus&amp;lt;/i&amp;gt; Fmb14 Ameliorate Fructose-Induced Hyperuricemia and Fatty Liver via Gut Modulation.</name><description>Fructose dietary intake is one of the most common risk factors for hyperuricemia, which is a critical threat to human health, and the lack of an effective biological intervention method is the main problem in preventing hyperuricemia caused by fructose intake. &lt;i>Lacticaseibacillus rhamnosus&lt;/i> Fmb14 (&lt;i>L. rhamnosus&lt;/i> Fmb14) has a fructose-metabolizing ability to produce extracellular polysaccharides (EPSs), and the yield of EPSs reached 0.50 and 0.42 g/L after 48 h of fermentation in liquid media of glucose-MRS and fructose-MRS. Six pure polysaccharide components were obtained after purification. A hyperuricemic mouse model was subsequently established by feeding a 60% high-fructose diet with potassium oxyazinate for 8 weeks, and the results revealed that &lt;i>L. rhamnosus&lt;/i> Fmb14 and</description><dates><release>2026-01-01T00:00:00Z</release><publication>2026 Jan</publication><modification>2026-07-07T03:14:35.953Z</modification><creation>2026-07-07T03:09:50.636Z</creation></dates><accession>S-EPMC12896772</accession><cross_references><pubmed>41682997</pubmed><doi>10.3390/foods15030409</doi></cross_references></HashMap>