Altered Gut Microbiota in Children With Hyperuricemia
In adults, gut dysbiosis may contribute to the pathogenesis of gout. However, the characteristics of gut microbiota in children with hyperuricemia (HUA) in the absence of clinical gout have not been explored. This present study analyzed the gut microbiota in children with HUA as compared to controls...
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Veröffentlicht in: | Frontiers in endocrinology (Lausanne) 2022-04, Vol.13, p.848715 |
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Zusammenfassung: | In adults, gut dysbiosis may contribute to the pathogenesis of gout. However, the characteristics of gut microbiota in children with hyperuricemia (HUA) in the absence of clinical gout have not been explored.
This present study analyzed the gut microbiota in children with HUA as compared to controls (Con) and explored bacterial associations that may account for differences.
A total of 80 children were enrolled in this study; they were divided into HUA and Con according to the level of serum uric acid (UA). The composition of gut microbiota was investigated by 16S rRNA high-throughput sequencing.
Principal coordinate analysis revealed that gut microbiota of the HUA group was clustered together and separated partly from the Con group. There was no difference in alpha-diversity between the two groups. However, Spearman's correlation analysis revealed that serum UA level positively correlated with genera
, and
, and negatively associated with the producers of short-chain fatty acids (SCFAs), such as
, and
, and the sulfidogenic bacteria
The members of the genera
and
in the Con group were significantly more prevalent than the HUA subjects. Compared to the Con cohort, metabolic pathway predictions found that the superpathways of purine nucleotide
biosynthesis were decreased in HUA subjects, whereas the superpathway of purine deoxyribonucleoside de gradation was increased.
The composition of the gut microbiota in children with HUA differs from Con. Although causality cannot be established, modification in the microbiota that produces SCFA and sulfide may promote HUA. |
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ISSN: | 1664-2392 1664-2392 |
DOI: | 10.3389/fendo.2022.848715 |