内科学
内分泌学
前列腺
医学
下尿路症状
前列腺癌
睾酮(贴片)
芳香化酶
炎症
增生
人口
经尿道前列腺电切术
前列腺疾病
二氢睾酮
雄激素
激素
癌症
乳腺癌
环境卫生
作者
Bichen Xue,Shulin Wu,Christina Sharkey,Shahin Tabatabaei,Chin‐Lee Wu,Zhipeng Tao,Zhiyong Cheng,Douglas W. Strand,Aria F. Olumi,Zongwei Wang
标识
DOI:10.1038/s41391-020-0208-4
摘要
Our patient cohort revealed that obesity is strongly associated with steroid-5α reductase type 2 (SRD5A2) promoter methylation and reduced protein expression. The underlying mechanism of prostatic growth in this population is poorly understood. Here we addressed the question of how obesity, inflammation, and steroid hormones affect the development of benign prostatic hyperplasia (BPH). We used preadipocytes, macrophages, primary human prostatic stromal cells, prostate tissues from high-fat diet-induced obese mice, and 35 prostate specimens that were collected from patients who underwent transurethral resection of the prostate (TURP). RNA was isolated and quantified with RT-PCR. Genome DNA was extracted and SRD5A2 promoter methylation was determined. Sex hormones were determined by high-performance liquid chromatography–tandem mass spectrometry. Protein was extracted and determined by ELISA test. In prostatic tissues with obesity, the levels of inflammatory mediators were elevated. SRD5A2 promoter methylation was promoted, but SRD5A2 expression was inhibited. Inflammatory mediators and saturated fatty acid synergistically regulated aromatase activity. Obesity promoted an androgenic to estrogenic switch in the prostate. Our findings suggest that obesity-associated inflammation induces androgenic to estrogenic switch in the prostate gland, which may serve as an effective strategy for alternative therapies for management of lower urinary tract symptoms associated with BPH in select individuals.
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