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 rhamnosus Fmb14 (L. rhamnosus 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 L. rhamnosus Fmb14 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 of allobaculum, bacteroides, Lactobacilli prevotella, and clostridium, 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.