Abstract

Metabolic syndrome (MetS) and diabetes mellitus (DM) are increasingly recognized as important risk factors in 
the development and progression of benign prostatic hyperplasia (BPH), a common urological condition in aging 
men characterized by prostatic enlargement and lower urinary tract symptoms (LUTS). Although traditionally 
considered separate clinical entities, an expanding body of epidemiological and experimental evidence links 
metabolic dysfunction with prostatic growth through shared pathophysiological mechanisms including chronic 
systemic inflammation, hormonal alterations, insulin resistance, and oxidative stress. This review synthesizes 
current knowledge on how elements of MetS, particularly obesity, dyslipidemia, hypertension, and hyperglycemia, 
intersect with diabetes-related biochemical pathways to influence prostatic cellular proliferation and stromal 
remodeling. We discuss the roles of insulin/insulin-like growth factor (IGF) signaling, adipokines, sex steroids, 
and inflammatory mediators in modulating prostatic epithelial and stromal dynamics. Converging evidence 
suggests that diabetic metabolic disturbances not only increase the risk of BPH but may also contribute to faster 
symptom progression and reduced therapeutic responsiveness. Understanding these interconnected pathways is 
critical for developing more effective preventive and therapeutic strategies. We conclude by outlining potential 
molecular targets and clinical implications for managing BPH in men with MetS and diabetes.