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 <i>Lactiplantibacillus plantarum</i> LP220 with kiwifruit powder and evaluated its effects in <i>vitro</i> and in an adenine and potassium oxonate mouse HUA model (8 weeks). In <i>vitro</i>, LP220 produced propionate 2.528 ± 0.369 μg/10⁹ CFU/mL and butyrate 36.06 ± 2.353 μg/10⁹ CFU/mL. In <i>vivo</i>, the synbiotic lowered serum uric acid by 62.27% versus untreated HUA (<i>P</i> < 0.01) and outperformed LP220 or kiwifruit alone, increasing fecal/serum and urinary/serum uric acid ratios by 242.99 and 117.49% (<i>P</i> < 0.01). Fecal and serum propionate and butyrate rose 38.01-129.34% (<i>P</i> < 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.