Frontiers in nutrition · 2026
Oral L-carnitine supplementation lowers serum uric acid and is associated with renal and intestinal urate-handling responses in hyperuricemic mice.
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Jin Fengyu, Huang Yujiao, Zhang Fengwei, He Jing, Zheng Jia, Jiang Minghui, Jiao Jiakang, Zhao Yinming, Liu Jinlian, Zhang Jianjun, Wang Linyuan
Аннотация
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.
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.