SCFAs-Enriching Kiwifruit-Derived Synbiotic Reprograms Microbiota to Suppress XOD and Promote Urate Clearance

Gut dysbiosis contributes to hyperuricemia (HUA), yet plant-based synbiotics that boost short-chain fatty acids (SCFAs) are underexplored. We developed a kiwifruit-derived synbiotic combining Lactiplantibacillus plantarum LP220 with kiwifruit powder and evaluated its effects in vitro and in an adenine and potassium oxonate mouse HUA model (8 weeks). In vitro, LP220 produced propionate 2.528 ± 0.369 μg/10 9 CFU/mL and butyrate 36.06 ± 2.353 μg/10 9 CFU/mL. In vivo, the synbiotic lowered serum uric acid by 62.27% versus untreated HUA ( P < 0.01) and outperformed LP220 or kiwifruit alone, increasing fecal/serum and urinary/serum uric acid ratios by 242.99 and 117.49% ( P < 0.01). Fecal and serum propionate and butyrate rose 38.01–129.34% ( P < 0.01), accompanied by reduced systemic inflammation (serum LPS – 38.81%; IL-1β – 23.74%). Mechanistically, the synbiotic decreased hepatic xanthine oxidase activity and upregulated ABCG2 expression in colon and kidney, with recovery of gut diversity and enrichment of SCFAs-producers. These results indicate the kiwifruit synbiotic suppresses urate synthesis and promotes excretion via SCFA-mediated microbiota–host interactions, suggesting a microbiota-targeted nutritional strategy for HUA.