ArticleFrontiers in nutrition2026
Oral L-carnitine supplementation lowers serum uric acid and is associated with renal and intestinal urate-handling responses in hyperuricemic mice.
Article in Frontiers in nutrition, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Hyperuricemia (HUA) is a common metabolic disorder associated with gout, renal dysfunction, and intestinal microenvironment disturbance. Impaired urate excretion is considered a major driver of sustained HUA. However, whether nutritional interventions are associated with renal and intestinal urate-handling-related responses remains unclear. This exploratory study investigated whether oral L-carnitine supplementation reduces serum uric acid levels and is accompanied by renal, intestinal, and microbiota-related changes. Methods: Male C57BL/6 mice were fed a UA/PO-supplemented diet for 12 weeks to establish the HUA model. Mice were assigned to a control group, an untreated HUA group, and L-carnitine-treated groups. Serum uric acid and renal-related biochemical indices were measured. Renal and intestinal histology, urate transporter expression, renal signaling pathways, and gut microbiota composition were evaluated to characterize hepatic urate production-related and renal-intestinal urate-handling-related responses. Results: Oral L-carnitine supplementation reduced serum uric acid levels and improved renal-related biochemical indices. It did not significantly affect hepatic XOD or ADA, indicating that the urate-lowering effect was not primarily explained by reduced hepatic urate production. In the kidney, L-carnitine restored OAT1 expression and attenuated NF-κB-related inflammatory signaling. In the intestine, it improved villus structure, increased ZO-1 and Occludin expression, and was associated with increased intestinal ABCG2 expression. Gut microbiota structure was also partially restored. Conclusion: These findings suggest that oral L-carnitine may act as a potential nutritional modulator of urate homeostasis. Its urate-lowering effect was not accompanied by detectable suppression of hepatic urate production, but was associated with renal and intestinal urate-handling-related responses. However, because standardized 24-h urinary and fecal urate excretion measurements and transporter functional assays were not performed, enhanced renal or intestinal urate excretion was not demonstrated.
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