Probiotics strategies for ameliorating hyperuricemia are promising based on the characteristics of probiotics and uric acid metabolism in humans. The administration of probiotics could ameliorate hyperuricemia and its related metabolic disorders.

Surfactin from Bacillus amyloliquefaciens fmb50 was utilized to treat mice with type 2 diabetes (T2DM) induced by a high-fat diet/streptozotocin (HFD/STZ). Our group’s earlier research indicated that surfactin could lower blood glucose and mitigate liver dysfunction to further improve HFD/STZ-induced T2DM through modulating intestinal microbiota. Thus, we further investigated the effects of surfactin on the pancreas and colon in mice with T2DM to elucidate the detailed mechanism. In the present study, mice with HFD/STZ-induced T2DM had their pancreatic and colon inflammation, oxidative stress, and endoplasmic reticulum stress (ERS) reduced when given oral surfactin at a dose of 80 mg/kg body weight. According to further research, surfactin also improved glucose metabolism by activating the phosphatidylinositol kinase (PI3K)/protein kinase B (Akt) signaling pathway, further protecting islets β-cell, promoting insulin secretion, inhibiting glucagon release and mitigating pancreas dysfunction. Additionally, after surfactin treatment, the colon levels of the tight junction proteins Occludin and Claudin-1 of T2DM mice were considerably increased by 130.64% and by 36.40%, respectively. These findings revealed that surfactin not only ameliorated HFD/STZ-induced pancreas inflammation and dysfunction and preserved intestinal barrier dysfunction and gut microbiota homeostasis but also enhanced insulin sensitivity and glucose homeostasis in T2DM mice. Finally, in the further experiment, we were able to demonstrate that early surfactin intervention might delay the development of T2DM caused by HFD/STZ, according to critical biochemical parameters in serum.

Prevention mechanism of L. rhamnosus Fmb14 on DSS-induced depression-like behaviors.

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.