Hypothesis / aims of study
Recently, the concept of “lipid quality” has attracted increasing attention, particularly in the context of metabolic syndrome characterized by chronic inflammation within adipose tissue. Lipid quality provides a more comprehensive index of adipose tissue pathology, and its decline has been associated with diabetes, nonalcoholic fatty liver disease, and atherosclerosis. However, its role in benign prostatic enlargement (BPE) and lower urinary tract symptoms (LUTS) remains insufficiently elucidated. Therefore, this study aimed to investigate whether a decline in lipid quality—defined by adipocyte hypertrophy, chronic inflammation within adipose tissue, and ectopic fat deposition—in periprostatic and intraprostatic tissues is associated with the pathophysiology of BPE and LUTS.
Study design, materials and methods
This study included 50 patients who underwent robot-assisted radical prostatectomy for localized prostate cancer to acquire prostatic specimens and periprostatic adipose tissue. Periprostatic fat tissue obtained during surgery and non-cancerous prostate tissue specimens were histologically evaluated. Decline in lipid quality was assessed using multiple pathological parameters: adipocyte diameter in pre-prostatic fat, Crown-Like Structure (CLS) formation in pre-prostatic fat (Figure 1) as an indicator of chronic adipose tissue inflammation, and ectopic fat deposition within non-cancerous prostate tissue (Figure 2). In addition, immunohistochemical staining was performed to evaluate macrophage polarization, and the densities of M1 and M2 macrophages were quantified. Adipocyte diameter was measured microscopically in representative fields, and CLS was defined as macrophage aggregation surrounding adipocytes. Prostate volume was assessed preoperatively, and LUTS severity was evaluated using the International Prostate Symptom Score (IPSS), including total score and storage and voiding subscores. Associations between pathological lipid quality markers, prostate volume, and LUTS parameters were statistically analyzed.
Results
CLS were observed in 30% of patients (15/50), and ectopic fat deposition within the prostate was identified in 42% (21/50). A significant positive correlation was found between adipocyte diameter and prostate volume (r=0.38, p=0.007). Prostate volume was also significantly larger in patients with CLS than in those without CLS (p<0.001). Although the difference did not reach statistical significance (p=0.08), prostate volume tended to be larger in patients with ectopic fat deposition. Immunohistochemical analysis demonstrated a significant predominance of M1 macrophages over M2 macrophages (M1: 51.0 ± 6.7/mm² vs M2: 46.0 ± 5.2/mm², p=0.01).
No significant associations were found between adipocyte diameter and total IPSS or either subscore. Similarly, the presence of CLS was not significantly associated with total IPSS, storage symptoms, or voiding symptoms. However, patients with ectopic fat deposition demonstrated a significantly higher storage symptom subscore (p=0.03), whereas no significant association was observed with voiding symptoms.
Interpretation of results
Adipocyte hypertrophy, CLS formation, and M1-dominant macrophage polarization in periprostatic fat were associated with prostate enlargement, suggesting that impaired lipid quality may promote prostatic growth through a pro-inflammatory microenvironment. In addition, intraprostatic ectopic fat deposition showed a closer relationship with urinary storage symptoms, indicating that local fat infiltration within the prostate may differentially contribute to symptom manifestation. These findings support the concept that distinct components of lipid quality decline—periprostatic inflammation and intraprostatic fat deposition—may play complementary roles in the pathogenesis of BPE and LUTS.