Metabolic and microbial crossroads: Sodium-glucose cotransporter-2 inhibitors and urinary tract infections in (Asian) diabetes care

The global rise of type 2 diabetes, particularly in Asian populations, has led to widespread adoption of sodium-glucose cotransporter-2 (SGLT2) inhibitors for glycemic control. While effective, these agents elevate the risk of urinary tract infections (UTIs) by inducing glycosuria, which creates a nutrient-rich environment that favors uropathogen growth. Asian individuals may be disproportionately vulnerable to SGLT2 inhibitor–associated UTIs due to a confluence of factors, including lower body mass index, increased visceral adiposity, congenital urinary tract anomalies, and genetic polymorphisms that impair uroepithelial integrity and immunity. This review integrates emerging evidence on the molecular, anatomical, and immunometabolic mechanisms that underlie infection susceptibility in this population. Special attention is given to the role of Escherichia coli virulence pathways—including adhesin expression, siderophore production, and biofilm formation—along with host immune impairments in diabetes that facilitate infection persistence. The review also explores how recurrent antibiotic use in these settings accelerates antimicrobial resistance, particularly among extended-spectrum β-lactamase -producing strains. Targeted public health strategies—encompassing glycemic control, antimicrobial stewardship, and non-antibiotic therapies—are needed. This synthesis provides a framework for developing personalized, regionally informed approaches to UTI prevention and management in high-risk diabetic Asian populations.