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Peer-reviewed veterinary case report

Oral supplementation ofSMM847 ameliorates hyperuricemia in rats and alcohol-induced injury in mice.

Journal:
Applied and environmental microbiology
Year:
2026
Authors:
Cao, Yuxin et al.
Affiliation:
College of Life Sciences · China
Species:
rodent

Abstract

UNLABELLED: Excessive dietary purine intake can lead to hyperuricemia, facilitating the precipitation and deposition of monosodium urate crystals in joints, which subsequently triggers inflammatory cascades leading to gout. Alcohol consumption exacerbates this condition by accelerating purine metabolism and impairing renal uric acid excretion, thereby further increasing serum uric acid concentrations and aggravating gout severity. In this study,SMM847 was screened based on its inosine degradation efficiency. Notably, the strain SMM847 also exhibited alcohol dehydrogenase and aldehyde dehydrogenase activities, as well as a substantial capability for ethanol degradation. In a hyperuricemic rat model, administration of SMM847 significantly reduced serum uric acid levels. Furthermore, in an ethanol-stressed mouse model, SMM847 markedly decreased blood ethanol concentrations, restored hepatic metabolic function, and enhanced endogenous antioxidant capacity, thereby counteracting ethanol-induced disturbances in nutrient absorption and systemic metabolism. Importantly, SMM847 showed no hepatotoxicity and effectively mitigated alcohol-induced histopathological liver injury. By concurrently targeting hyperuricemia and acute alcohol intoxication, this study identifies SMM847 as a promising probiotic candidate for the management of gout and alcohol-related metabolic disorders. IMPORTANCE: This study presents the probiotic strainSMM847 as a promising therapeutic agent for two clinically significant conditions: hyperuricemia and acute alcohol intoxication. The strain mediates uric acid reduction through modulation of purine catabolism pathways. It is particularly noteworthy that SMM847 exhibits ethanol-catabolizing activity, attenuates alcohol-elicited systemic metabolic dysregulation, and exerts hepatoprotection without intrinsic toxicity. The ability of this single bacterial entity to simultaneously target dual pathological pathways-uric acid metabolism and alcohol-induced metabolic disruption-offers a novel and translatable approach for the development of functional foods or pharmaceutical interventions aimed at promoting integrated metabolic and hepatic health.

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Original publication: https://pubmed.ncbi.nlm.nih.gov/41848409/