This study investigates the causal relationship between obesity and hyperuricemia using mendelian randomization (MR) and network pharmacology. The MR analysis, based on genome-wide association study (GWAS) summary statistics, indicates a positive causal association between body mass index (BMI) and hyperuricemia, with an odds ratio of 1.23 per standard deviation increase in BMI. However, hyperuricemia does not significantly influence BMI. Sensitivity analyses confirmed the robustness of these findings, showing no significant horizontal pleiotropy or heterogeneity. Network pharmacology analysis identified 235 common targets between obesity and hyperuricemia, with insulin resistance as the top key target. Pathway enrichment analysis revealed that important pathways, including adipocytokine signaling, insulin resistance, and cholesterol metabolism, are involved in the mechanism linking obesity and hyperuricemia. Insulin resistance is proposed as a key link in this pathway network. The study concludes that obesity leads to hyperuricemia through insulin resistance, which is a critical pathway in the complex network of mechanisms underlying the association between obesity and hyperuricemia. The findings support the use of MR and network pharmacology to understand the causal relationships and mechanisms between obesity and hyperuricemia, providing a theoretical basis for the clinical treatment of hyperuricemia in obese patients.This study investigates the causal relationship between obesity and hyperuricemia using mendelian randomization (MR) and network pharmacology. The MR analysis, based on genome-wide association study (GWAS) summary statistics, indicates a positive causal association between body mass index (BMI) and hyperuricemia, with an odds ratio of 1.23 per standard deviation increase in BMI. However, hyperuricemia does not significantly influence BMI. Sensitivity analyses confirmed the robustness of these findings, showing no significant horizontal pleiotropy or heterogeneity. Network pharmacology analysis identified 235 common targets between obesity and hyperuricemia, with insulin resistance as the top key target. Pathway enrichment analysis revealed that important pathways, including adipocytokine signaling, insulin resistance, and cholesterol metabolism, are involved in the mechanism linking obesity and hyperuricemia. Insulin resistance is proposed as a key link in this pathway network. The study concludes that obesity leads to hyperuricemia through insulin resistance, which is a critical pathway in the complex network of mechanisms underlying the association between obesity and hyperuricemia. The findings support the use of MR and network pharmacology to understand the causal relationships and mechanisms between obesity and hyperuricemia, providing a theoretical basis for the clinical treatment of hyperuricemia in obese patients.