Exopolysaccharides from Lacticaseibacillus rhamnosus Fmb14 Ameliorate Fructose-Induced Hyperuricemia and Fatty Liver via Gut Modulation

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.Lacticaseibacillus rhamnosusFmb14 (L. rhamnosusFmb14) 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 thatL. rhamnosusFmb14 and fructose-derived EPS (F-EPS) intervention significantly reduced the serum uric acid level of the model mice from 133.6 μmol/L to 106.7 to 111.0 μmol/L. The content of XOD in the liver decreased from 2188.1 ng/L in the model group to 1797.9 ng/L in the H-Fmb14 group and 1906.6 ng/L in the H-F-EPS group, alleviating fatty liver degeneration and improving intestinal barrier (increasing OCLN and ZO1 expression in colon). The abundances ofallobaculum,bacteroides,Lactobacilli prevotella, andclostridium, the new potential biomarkers of fructose-induced hyperuricemia, were found to be modulated after Fmb14 and F-EPS intervention. The effects of Fmb14 and F-EPS in reducing uric acid synthesis and protecting the intestinal tract are very promising as food intervention agents in the prevention of hyperuricemia caused by fructose dietary.