ABSTRACT
Hyperuricemia is closely linked with an increased risk of developing hypertension, diabetes, renal failure and other metabolic syndromes. Probiotics, bioactive compounds and dietary patterns are safe cost-efficient ways to control hyperuricemia, whereas comprehensive reviews of their anti-hyperuricemic mechanisms are limited. This review summarizes the roles of probiotics, bioactive compounds and dietary patterns in treating hyperuricemia and critically reviews the possible mechanisms by which these interventions exert their activities. The dietary patterns are closely related to the occurrence of hyperuricemia through the indirect action of gut microbiota or the direct effects of host purine metabolism. The Mediterranean and Dietary Approaches to Stop Hypertension diets help reduce serum uric acid concentrations and thus prevent hyperuricemia. Meanwhile, probiotics alleviate hyperuricemia by ways of absorbing purine, restoring gut microbiota dysbiosis and inhibiting xanthine oxidase (XO) activity. Bioactive compounds such as polyphenols, peptides and alkaloids exert various anti-hyperuricemic effects, by regulating urate transporters, blocking the active sites of XO and inhibiting the toll-like receptor 4/nuclear factor kappa B signaling pathway and NOD-, LRR- and pyrin domain-containing protein 3 signaling pathway. This review will assist people with hyperuricemia to adopt a healthy diet and contribute to the application of natural products with anti-hyperuricemic activity.
ABSTRACT
Globally, the incidence of hyperuricaemia is steadily increasing. The evidence increasingly suggests an association between hyperuricaemia and the gut microbiota, which may enable the development of a novel therapeutic approach. We studied the effects of treatment with lactic acid bacteria (LAB) on hyperuricaemia and their potential underlying mechanisms. A mouse model of hyperuricaemia was generated by oral gavage with hypoxanthine and intraperitoneal injections of potassium oxonate for 2 weeks. The anti-hyperuricaemic activities of 10 LAB strains relative to allopurinol as a positive drug control were investigated in the mouse model. Lactobacillus rhamnosus R31, L. rhamnosus R28-1 and L. reuteri L20M3 effectively reduced the uric acid (UA) concentrations in serum and urine and the xanthine oxidase (XOD) activity levels in serum and hepatic tissue in mice with hyperuricaemia. These strains also reversed the elevated lipopolysaccharide (LPS) concentration, hepatic inflammation and slight renal injury associated with hyperuricaemia. A correlation analysis revealed that UA-reducing LAB strains promoted short-chain fatty acid (SCFA) production to suppress serum and hepatic XOD activity by increasing the abundances of SCFA production-related gut bacterial taxa. However, the UA-reducing effects of LAB strains might not be mediated by purine degradation. In summary, L. rhamnosus R31, L. rhamnosus R28-1 and L. reuteri L20M3 relieved hyperuricaemia in our mouse model by promoting SCFA production in a purine degradation-independent manner. Our findings suggest a novel therapeutic approach involving LAB strains for hyperuricaemia.
