Endocrine Abstracts (2013) 32 P655 | DOI: 10.1530/endoabs.32.P655

Fat boosts, while androgen receptor activation counteracts, BPH-associated prostate inflammation

Linda Vignozzi1, Mauro Gacci4, Ilaria Cellai1, Raffaella Santi5, Giovanni Corona2,1, Annamaria Morelli6, Giulia Rastrelli1, Paolo Comeglio1, Arcangelo Sebastianelli4, Elena Maneschi1, Gabriella Nesi5, Cosimo De Nunzio3, Andrea Tubaro3, Edoardo Mannucci7, Marco Carini4 & Mario Maggi1


1Sexual Medicine and Andrology Unit, University of Florence, Florence, Italy; 2Endocrinology Unit, Azienda Usl, Maggiore Bellaria Hospital, Bologna, Italy; 3Ospedale Sant’Andrea, University La Sapienza, Rome, Italy; 4Urology Unit, University of Florence, Florence, Italy; 5Pathological Anatomy Unit, University of Florence, Florence, Italy; 6Department of Experimental and Clinical Medicine, University of Florence, Florence, Italy; 7Diabetic Section Geriatric Unit, University of Florence, Florence, Italy.


Background: Metabolic syndrome (MetS) and benign prostate hyperplasia (BPH) are often comorbid. Chronic inflammation, a determinant pathogenic factor for BPH, is a putative link between the two conditions.

Methods: In a multi-center cohort of BPH patients (n=244) who underwent prostatectomy, we evaluated whether MetS is associated with prostatic inflammation in BPH specimens. In addition, we investigated the in vitro inflammatory effects of metabolic insults on human prostatic myofibroblastic cells (hBPH).

Results: Inflammatory infiltrates score (IS) in prostatectomy specimens showed a step-wise association with the number of MetS factors present (P=0.001). After adjusting for age, reduced HDL cholesterol and elevated triglycerides were the only factors significantly associated with IS. Increased IS was also significantly associated with hypogonadism. In an age- and testosterone (T) -adjusted model, dyslipidaemia was still associated with IS.

To investigate whether metabolic factors could directly trigger prostate inflammation, we performed preliminary studies in myofibroblastic hBPH. Among the different factors, oxidized low-density lipoprotein (oxLDL) showed the highest secretion of IL-8 (>10-folds) – a surrogate marker of prostate inflammation-as well as IL-6, and bFGF. Co-treatment with DHT significantly inhibited oxLDL-induced secretion of IL-8, whilst an AR-antagonist, bicalutamide, reversed DHT effects. DHT suppresses oxLDL receptor (LOX-1) expression.

Conclusions: Our data suggest that fats and insulin could have a detrimental effect on prostate health, boosting inflammation, a key pathogenic factor in BPH. Conversely, beneficial effects of DHT in counteracting lipid- and insulin-induced prostatic alterations, suggest that T – via its conversion into DHT – may have unexpected beneficial effects on prostate health.