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. 2025 Aug 5:16:1599107.
doi: 10.3389/fmicb.2025.1599107. eCollection 2025.

Therapeutic effect of fecal microbiota transplantation on hyperuricemia mice by improving gut microbiota

Songjian Yuan  1 , Wenting Jia  1 , Xiaomei Liu  1 , Ruzhen Liu  2 , Man Cao  2 , Yuting Wu  2 , Yuantao Li  2 , Wei Xu  2 , Chuanxing Xiao  1   2 , Zhenqiang Hong  1 , Bangzhou Zhang  1   2
Affiliations

Therapeutic effect of fecal microbiota transplantation on hyperuricemia mice by improving gut microbiota

Songjian Yuan et al. Front Microbiol. .

Abstract

Objective: The primary objective of this study was to assess the impact of fecal microbiota transplantation (FMT) on serum biochemical parameters, renal injury, and gut microbiota in hyperuricemia (HUA) mice.

Methods: Six-week-old male C57BL/6 J mice were given a high-purine diet and potassium oxonate injections to induce HUA, followed by a two-week FMT treatment. Regular body weight checks, serum biochemical analyses, and fecal sampling for 16S rRNA gene sequencing were conducted to evaluate the treatment's impact on gut microbiota.

Results: The model group showed significant increases in uric acid (UA), creatinine (Cr), blood urea nitrogen (BUN) levels, and increased xanthine oxidase (XOD) activity compared to controls (p < 0.05). FMT treatment effectively reduced these levels and XOD activity (p < 0.05). At the genus level, specific taxa like Muribaculaceae and Prevotellaceae_UCG-001 were less abundant, while Blautia and Ruminiclostridium_9 were more abundant in the model group. Following FMT, gut microbiota composition returned to near-normal levels, with significant differences from the model group (p < 0.05).

Conclusion: This study demonstrates that FMT holds therapeutic potential for HUA mice by reducing UA levels, alleviating renal damage, and restoring gut microbiota balance.

Keywords: fecal microbiota transplantation; gut microbiota; hyperuricemia; microbiome; renal injury.

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Conflict of interest statement

RL, MC, YW, YL, WX, CX, and BZ were employed by Xiamen Treatgut Biotechnology Co., Ltd. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Experimental chart in the treatment of HUA mice.
Figure 2
Figure 2
(A) Body weight (n = 6). (B) Concentration of UA from each group. (C) Activity of XOD from each group. (D) Concentration of creatinine from each group. (E) Concentration of BUN from each group. Data are presented as mean ± SD. *** p < 0.001, ** p < 0.01 and * p < 0.05 vs. the MOD group. ### p < 0.001 vs. the CON group.
Figure 3
Figure 3
Histopathological analyses of H&E stained kidney sections (×400 magnification) from mice.
Figure 4
Figure 4
FMT alters the structure of the gut microbiota in hyperuricemic mice. (A) Venn diagram; (B) Alpha diversity based on the Shannon diversity index, the Simpson diversity index, and the inverse Simpson diversity index (J) in groups of mice.
Figure 5
Figure 5
FMT alters the structure of the gut microbiota in hyperuricemic mice. (A) Non-metric multidimensional scaling plot (NMDS); (B) β-diversity based on the Bray-Curtis PCoA method analysis.
Figure 6
Figure 6
The taxonomic compositions of the gut microbiota in hyperuricemia mice. Relative abundance of the gut microbial community in each group at (A) The phylum level. (B) The genus level.
Figure 7
Figure 7
Effect of FMT on the gut microbiota at the genus level in hyperuricemic mice. (A) Heat maps of most of the selected differential features at the genus level; (B) Differences in gut microbiota composition at various levels derived from LEfSe analyses.
Figure 8
Figure 8
Box plots of genus-level differential species in each group.
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