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Diabetes mellitus is a significant risk factor for urinary tract infections (UTIs), which occur more frequently, have a more severe course, and show a greater tendency to recur in affected individuals. Metabolic disturbances, particularly hyperglycemia and glucosuria, promote bacterial growth while simultaneously impairing innate and adaptive immune responses. In addition, diabetes-related complications, such as autonomic neuropathy, contribute to bladder dysfunction and urinary stasis, further facilitating bacterial colonization. Epidemiological evidence indicates a two- to four-fold increased risk of UTIs in patients with diabetes, along with a high prevalence of asymptomatic bacteriuria and recurrent infections. A key feature of this relationship is its bidirectional nature. UTIs can exacerbate glycemic dysregulation by triggering stress responses and increasing insulin resistance, leading to transient or sustained hyperglycemia. Uropathogenic Escherichia coli plays a critical role in the pathogenesis of UTIs, with hyperglycemic conditions further enhancing bacterial adhesion, biofilm formation, and immune evasion. Effective management requires simultaneous control of infection and optimization of glycemic control, particularly in the context of rising antimicrobial resistance. Emerging therapeutic strategies include targeting bacterial adhesion, disrupting biofilms, and modulating host immune responses. Improved understanding of host-pathogen interactions may enable the development of more effective preventive and therapeutic approaches in this high-risk population.