Nutrition, metabolism, and cardiovascular diseases : NMCD · 2026
Hyperuricemia, gout and obesity: should weight management be more of a focus in gout management?
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Scilletta Sabrina, Di Marco Maurizio, Bosco Giosiana, Di Giacomo Barbagallo Francesco, Galeano Francesco, Tumminia Andrea, Milluzzo Agostino, Gaudio Agostino, Frittitta Lucia, Scicali Roberto, Castellino Pietro, Piro Salvatore, Sattar Naveed, Di Pino Antonino
Аннотация
AIMS: Hyperuricemia-elevated serum uric acid (SUA)-is the pathogenic driver of gout and is recognized as a systemic condition associated with cardiometabolic risk, including cardiovascular disease and type 2 diabetes, although causality remains debated. Its global prevalence has risen substantially over decades, paralleling the growing epidemic of obesity and increasing life expectancy. This narrative review examines the relationship between adiposity and hyperuricemia and summarises the knowledge about the impact of weight-loss interventions on SUA levels and gout risk.
DATA SYNTHESIS: Epidemiological evidence supports a bidirectional relationship between adiposity and hyperuricemia, although Mendelian randomisation studies suggest that excess adiposity is likely a cause rather than consequence of elevated SUA. Multiple mechanisms may underlie this association, including insulin resistance, reduced renal urate excretion, visceral adiposity, and dietary factors. Weight reduction is now recommended as a cornerstone of hyperuricemia and gout management in individuals with overweight or obesity. Lifestyle and dietary interventions are associated with modest reductions in SUA and gout risk. Bariatric surgery achieves substantial and sustained weight loss, leading to significant long-term reductions of SUA and gout incidence, despite a transient postoperative SUA increase. Recently, pharmacological weight-loss therapies (i.e. glucagon-like peptide-1 receptor agonists and tirzepatide) demonstrated meaningful reductions in SUA levels, potentially largely mediated by weight loss.
CONCLUSIONS: Integrating obesity management into hyperuricemia care represents a key strategy to reduce gout incidence and flares. Further research evaluating emerging anti-obesity therapies impact on hyperuricemia-specific outcomes would be useful, perhaps particularly in people experiencing ongoing flares despite other therapies and with obesity.
DATA SYNTHESIS: Epidemiological evidence supports a bidirectional relationship between adiposity and hyperuricemia, although Mendelian randomisation studies suggest that excess adiposity is likely a cause rather than consequence of elevated SUA. Multiple mechanisms may underlie this association, including insulin resistance, reduced renal urate excretion, visceral adiposity, and dietary factors. Weight reduction is now recommended as a cornerstone of hyperuricemia and gout management in individuals with overweight or obesity. Lifestyle and dietary interventions are associated with modest reductions in SUA and gout risk. Bariatric surgery achieves substantial and sustained weight loss, leading to significant long-term reductions of SUA and gout incidence, despite a transient postoperative SUA increase. Recently, pharmacological weight-loss therapies (i.e. glucagon-like peptide-1 receptor agonists and tirzepatide) demonstrated meaningful reductions in SUA levels, potentially largely mediated by weight loss.
CONCLUSIONS: Integrating obesity management into hyperuricemia care represents a key strategy to reduce gout incidence and flares. Further research evaluating emerging anti-obesity therapies impact on hyperuricemia-specific outcomes would be useful, perhaps particularly in people experiencing ongoing flares despite other therapies and with obesity.