Fecal SCFA profiles differed across the clinical spectrum of hyperuricemia in Mexican adults, with a disease-specific association between dietary purine intake and fecal acetate and a gout-specific link between Prevotella spp. abundance and acetate, suggesting a disease-specific gut metabolic response to dietary purines that may contribute to the inflammatory environment of established gout.
Fecal acetate and propionate concentrations were significantly higher in gout patients than in normouricemic controls.
Individuals with asymptomatic hyperuricemia had significantly higher fecal butyrate than the comparison groups.
Moderate-purine food intake had opposing associations with fecal acetate in controls and gout patients.
In exploratory analyses, Prevotella spp. abundance was positively associated with fecal acetate only in the gout group.
The authors conclude that a disease-specific gut metabolic response to dietary purine intake may contribute to the inflammatory environment of established gout, but causality cannot be established with this design.
This study compared stool samples and diets of 380 Mexican adults: people with normal uric acid levels, people with high uric acid but no symptoms, and people with gout. The researchers measured short-chain fatty acids, which are compounds made by gut bacteria that can influence inflammation, and looked at two bacterial groups, Akkermansia and Prevotella. People with gout had higher stool levels of acetate and propionate than people with normal uric acid, while people with symptom-free high uric acid had higher butyrate. Eating moderate-purine foods was linked to higher acetate in healthy controls but lower acetate in people with gout, suggesting the gut may respond differently to dietary purines depending on disease status. Prevotella abundance was linked to acetate only in the gout group, though this was an exploratory finding. These results suggest that gut-derived metabolites differ across stages of high uric acid and gout, and may be related to inflammation in gout. Because the study captured a single point in time and measured only selected bacteria, it cannot show that these differences cause disease. Longer-term studies that profile the whole microbiome are needed.
Fuentes-Bello A, Guevara-Gonzalez K, Granados-Portillo O, Sánchez-Lozada L, Jasso-Chávez R, Galeana-Cadena D, et al.. (2026). Associations Between Gut Microbiota Abundance, Dietary Purine Intake, and Fecal Short-Chain Fatty Acids Across the Clinical Spectrum of Hyperuricemia: A Cross-Sectional Study in Mexican Adults.. Nutrients. https://doi.org/10.3390/nu18203326