The Role of Periprostatic Adipose Tissue on Prostate Function in Vascular-Related Disorders

The lower urinary tract symptoms (LUTS) secondary to benign prostatic hyperplasia (BPH) are highly prevalent worldwide. Clinical and experimental data suggest that the incidence of LUTS-BPH is higher in patients with vascular-related disorders such as in pelvic ischemia, obesity and diabetes as well as in the ageing population. Obesity is an important risk factor that predisposes to glucose intolerance, insulin resistance, dyslipidemia, type 2 diabetes mellitus and cardiovascular disorders. Prospective studies showed that obese men are more likely to develop LUTS-BPH than non-obese men. Yet, men with greater waist circumferences were also at a greater risk of increased prostate volume and prostate-specific antigen than men with lower waist circumference. BPH is characterized by an enlarged prostate and increased smooth muscle tone, thus causing urinary symptoms. Data from experimental studies showed a significant increase in prostate and epididymal adipose tissue weight of obese mice when compared with lean mice. Adipose tissues that are in direct contact with specific organs have gained attention due to their potential paracrine role. The prostate gland is surrounded by periprostatic adipose tissue (PPAT), which is believed to play a paracrine role by releasing growth factors, pro-inflammatory, pro-oxidant, contractile and anti-contractile substances that interfere in prostate reactivity and growth. Therefore, this review is divided into two main parts, one focusing on the role of adipokines in the context of obesity that can lead to LUTS/BPH and the second part focusing on the mediators released from PPAT and the possible pathways that may interfere in the prostate microenvironment.

LUTS in pelvic ischemia: a new concept in voiding dysfunction

Lower urinary tract symptoms (LUTS) are a group of voiding symptoms affecting both genders as they age. Traditionally, LUTS in men were commonly attributed to bladder outlet obstruction (BOO) due to benign prostatic enlargement (BPE). It was later shown that, in approximately one-third to more than one-half of cases, LUTS in men are not associated with BOO. Urodynamic changes in the male bladder and symptom scores in aging men were found to be identical to their age-matched female counterparts. These observations suggested that LUTS in the elderly do not necessarily relate to BOO and may result from local changes in bladder muscle, nerves, and blood vessels. However, aging factors predisposing to bladder dysfunction and LUTS remain unknown. Growing evidence suggests that aging-associated pelvic ischemia may be a primary factor in the development of nonobstructed nonneurogenic overactive bladder and LUTS. First identified in experimental models and later in clinical studies, pelvic ischemia has been shown to compromise the lower urinary tract structure and lead to dysfunction. Structural and functional consequences of bladder and prostate ischemia have been documented in animal models. Clinical studies have shown that bladder and prostate blood flow decreases with aging. The severity of LUTS in elderly patients correlates with the degrees of bladder ischemia. LUTS improvement with α blockers has been associated with increased bladder blood flow. Pelvic ischemia may be an independent factor in nonobstructed nonneurogenic bladder instability and LUTS. Further research into the pathophysiology of LUTS in pelvic ischemia may lead to better management of this problem in the elderly population.