AI Article Synopsis
- About 15% of US adults have high uric acid levels linked to gout, while most mammals use the enzyme uricase to eliminate it, which humans lack due to evolutionary changes.
- Researchers discovered a bacterial gene cluster in the gut that can degrade uric acid into other compounds like xanthine and fatty acids.
- Removing gut bacteria in mice without uricase led to high uric acid levels, suggesting that gut microbiota play a role in uric acid excretion and indicating potential new treatments targeting the microbiome for hyperuricemia.
Article Abstract
Approximately 15% of US adults have circulating levels of uric acid above its solubility limit, which is causally linked to the disease gout. In most mammals, uric acid elimination is facilitated by the enzyme uricase. However, human uricase is a pseudogene, having been inactivated early in hominid evolution. Though it has long been known that uric acid is eliminated in the gut, the role of the gut microbiota in hyperuricemia has not been studied. Here, we identify a widely distributed bacterial gene cluster that encodes a pathway for uric acid degradation. Stable isotope tracing demonstrates that gut bacteria metabolize uric acid to xanthine or short chain fatty acids. Ablation of the microbiota in uricase-deficient mice causes severe hyperuricemia, and anaerobe-targeted antibiotics increase the risk of gout in humans. These data reveal a role for the gut microbiota in uric acid excretion and highlight the potential for microbiome-targeted therapeutics in hyperuricemia.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10421625 | PMC |
| http://dx.doi.org/10.1016/j.cell.2023.06.010 | DOI Listing |
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