Obesity is associated with a high prevalence of erectile dysfunction; however, the pathophysiological link between obesity and erectile dysfunction remains poorly understood. In this minireview, we have attempted to evaluate the existing literature pertaining to obesity and erectile dysfunction to determine whether a common pathophysiological link exists. Visceral obesity is associated with increased inflammatory responses, which contribute to endothelial dysfunction. Furthermore, obesity is also associated with reduced plasma testosterone levels, which contributes to hypogonadism and increases the risk of vascular pathology. Endothelial dysfunction and androgen deficiency have previously been linked to the pathophysiological mechanisms of erectile dysfunction. The underlying pathophysiological mechanisms of endothelial dysfunction and testosterone deficiency include penile vascular insufficiency as a result of the loss of nitric oxide synthase expression and activity and the loss of tissue compliance, resulting in reduced hemodynamic properties. Recent progress in the field of sexual medicine has recognized the impact of vascular disease and hypogonadism on the management of patients with erectile dysfunction. We suggest that visceral obesity, a component of the metabolic syndrome, adversely affects endothelial function and testosterone levels, contributing to hypogandism and erectile dysfunction. Thus, clinical screening for the risk of erectile dysfunction in obese patients should include the assessment of waist circumference, testosterone levels, body mass index and physical inactivity.