作者: Linda Vignozzi , Sandra Filippi , Paolo Comeglio , Ilaria Cellai , Annamaria Morelli
DOI: 10.1111/JSM.12695
关键词:
摘要: Abstract Introduction Estrogen receptor (ER) α is critical in mediating the harmful effects of hyperestrogenism fetal or neonatal life on developing penis. In contrast, little known impact an excess estrogens penile function adulthood. Aim To investigate effect metabolic syndrome (MetS)‐associated erectile dysfunction (ED). Methods We employed a recently established animal model high fat diet (HFD)‐induced MetS. Subgroups MetS rabbits were dosed with either testosterone (T) tamoxifen. evaluated responsiveness to acetylcholine (Ach) as well expression genes related smooth muscle relaxation and contractility. Main Outcome Measure Associations between MetS‐induced alterations sex steroids investigated HFD‐induced understand role androgen deficiency estrogen ED, we treated subgroups T tamoxifen, classical ER antagonist. Results Feeding was associated elevated estradiol (E2) low levels. E2, but not T, independently negatively able affect erection. Smooth muscle‐related markers decreased E2 positively all variables investigated. Increasing concentrations circulating Ach‐induced relaxation. HFD rabbits, vivo dosing significantly improved completely normalized E2. Conversely, tamoxifen reduced visceral adiposity partially restored level. severely impaired by restored, up control level, both dosing. rabbit cells cultures 17β‐E2 (1 nM) α‐smooth actin, transgelin, phosphodiesterase type 5. The reverted (100 nM). Conclusions This study demonstrates, for first time, that ED more rather than milieu. treatment only also nonsteroidal antagonist, Vignozzi L, Filippi S, Comeglio P, Cellai I, Morelli A, Marchetta M, Maggi M. mediates syndrome‐induced dysfunction: A rabbit. J Sex Med 2014;11:2890–2902.