The role of dietary polysaccharides in uric acid regulation: Mechanisms and benefits in managing hyperuricemia

Background

Hyperuricemia (HUA) is a systemic metabolic disorder caused by disturbances in purine metabolism. Persistent HUA can lead to the formation of urate crystals, which activate immune responses, causing joint tissue damage and the development of gout. Currently, clinical therapeutic drugs for HUA are associated with notable adverse side effects. Dietary polysaccharides, derived from various natural sources and forms, offer a safer and more sustainable therapeutic approach for managing HUA.

Scope and approach

This review discusses the pathogenesis of HUA, the metabolic characteristics and physiological functions of dietary polysaccharides, and the potential molecular mechanisms by which polysaccharides exert their uric acid-lowering effects.

Key findings and conclusions

Dietary polysaccharides from diverse sources improve HUA through several mechanisms: (1) Modulating key enzymes involved in uric acid production and metabolism, such as xanthine oxidoreductase and adenosine deaminase, as well as uric acid transporters like GLUT9, OAT1, OAT3, and ABCG2 in the liver, kidneys, and intestines to regulate uric acid production and excretion. (2) Regulating key signaling pathways, including TLR4/MyD88/NF-κB, TGF-β/Smad, and JAK/STAT, to reduce oxidative stress and inflammation. (3) Promoting the abundance of gut microbiota, such as Lactobacillus and Bifidobacterium, and regulating their metabolic products to maintain gut homeostasis. (4) Other mechanisms, including regulating the expression of LPCAT3, SREBP1, and PPARα, to improve lipid metabolism and liver function. Dietary polysaccharides hold significant potential as natural, safe, and effective supplements for the prevention and management of hyperuricemia.