Prostatic inflammation and obstructive voiding in the adult noble rat: Impact of the testosterone to estradiol ratio in serum

Bernoulli, Jenni; Yatkin, Emrah; Konkol, Yvonne; Talvitie, Eva-Maria; Santti, Risto; Streng, Tomi

doi:10.1002/pros.20791

Cited by 54 publications

(49 citation statements)

References 33 publications

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“…Investigations on animals confirm that changes in the physiological ratio of both hormones contribute to a gradual increase in the prostate volume and disturbances in urination [23]. Nevertheless, the study of Bernoulli et al [23] fails to confirm the hypothesis that a decrease in the ratio of testosterone to estradiol is associated with LUTS. However, Tao et al [24] found that patients with BPH had higher estradiol levels than patients without BPH.…”

Section: Discussionmentioning

confidence: 99%

Hormone concentration, metabolic disorders and immunoexpression of androgen and estrogen-alpha receptors in men with benign prostatic hyperplasia and testosterone deficiency syndrome

Rył

Rotter

Słojewski

et al. 2015

Folia Histochem Cytobiol.

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Introduction. A slight decrease in blood testosterone level in men is a physiological state associated with the aging. The aim of our study was to evaluate the occurrence of hormone and metabolic disorders, as well as the immunolocalization and immunoexpression of androgen receptors (AR) and estrogen-alpha receptors (ERa) in the prostates of men with benign prostatic hyperplasia (BPH) and coexisting testosterone deficiency syndrome (TDS). Material and methods. The study involved 150 men, diagnosed with and receiving pharmacological treatment for BPH. Concentrations of glucose, total cholesterol (TCh), high-density lipoproteins (HDL), low-density lipoproteins (LDL), and triglycerides (TG) were determined in blood serum. Serum concentrations of total testosterone (TT), free testosterone (FT), estradiol (E2), luteinizing hormone (LH), insulin (I), sex hormone-binding globulin (SHBG), dehydroepiandrosterone sulfate (DHEAS), and insulin-like growth factor 1 (IGF-1) were measured by ELISA. The number of AR-positive cells and ERa-positive cells were measured in prostate sections of men with BPH. Results. Patients eligible for transurethral resection of the prostate and TDS were significantly more likely to have higher abdominal circumference and higher serum levels of insulin and IGF-1 as well as lower levels of FT and SHBG than control subjects with BPH and no TDS. Quantitative analysis revealed 35.8% AR-positive columnar epithelial cells and 24.3% AR-positive stromal cells in prostates of BPH patients with TDS and 30.5% and 23.0%, respectively, in BPH patients without TDS. However, the differences between the study and the control groups were statistically not significant. In prostates of BPH patients with TDS the immunoexpression of ERa was observed in 2.88% of the columnar epithelial cells and 0.39% of stromal cells. In BPH patients without TDS ERa-positive cells were only found in 0.04% of columnar epithelial cells and 0.62% of prostatic stromal cells. Conclusions. Considering the statistically significantly higher levels of I and IGF-1 and larger abdominal circumference of men with BPH and TT deficiency, it can be supposed that visceral obesity and carbohydrate disorders may contribute to the reduction of testosterone concentration. The results of our study indicate a relationship between TT concentration in the plasma of patients with BPH and the percentage of AR-positive cells in the prostate.

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Section: Discussionmentioning

confidence: 99%

Hormone concentration, metabolic disorders and immunoexpression of androgen and estrogen-alpha receptors in men with benign prostatic hyperplasia and testosterone deficiency syndrome

Rył

Rotter

Słojewski

et al. 2015

Folia Histochem Cytobiol.

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“…17 Bernoulli et al showed that the reduction of the serum TT:E2 ratio is associated with onset of non-bacterial prostatitis without urodynamic alterations in the animal model with hypoandrogenism combined with hyperestrogenism, while obstructive disorders appeared in the hyperandrogenic animals with low serum TT:E2 ratio. 18 In another experimental model, chronic treatment with estrogens results in the activation of metalloproteinases 2,7,9 in the lateral lobe of the prostate and increase of leukocyte infiltrate. 19 Other conceivable causes could be represented by the functional alterations of aromatase, the enzyme responsible for the conversion of T into E2, which are more frequent in infertile patients, 20 or the TT reduction associated with the psychological stress which is another important characteristic of patients with chronic prostate inflammation.…”

Section: Discussionmentioning

confidence: 99%

Hyperestrogenism and low serum testosterone-17β-estradiol ratio are associated with non-bacterial male accessory gland inflammation

Condorelli

Calogero

Vignera

2016

Int J Immunopathol Pharmacol

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This study evaluated the serum concentrations of the main sex hormones in selected patients with non-bacterial male accessory gland infection (MAGI). The results suggest that the mean serum concentrations of 17β-estradiol (method : chemiluminescence) in these patients are significantly higher compared to the controls (55.0 ± 15.0 vs. 26.5 ± 12.0 pg/mL; P <0.05) and the percentage of patients with MAGI and associated hyperestrogenism (according to the laboratory range used in this study) was significantly higher (25.00% vs. 3.00%; P <0.05). Moreover, the percentage of patients with nonbacterial MAGI and associated testosterone deficiency (serum total testosterone <2.49 ng/mL) was significantly higher (18.00% vs. 2.00%; P <0.05). Finally, patients with non-bacterial MAGI showed a significantly lower total testosterone-17β-estradiol ratio compared to the controls (72.7 vs. 173.0; P <0.05). The results of this study, with some limitations (in particular the method applied for the determination of serum concentrations of 17β-estradiol) represent in our opinion, a topic worthy of further investigation for a correct endocrinological characterization of these patients, useful for clinical practice.

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“…In contrast, in a rat study with E2 treatment plus different doses of T, obstructive voiding was only observed in treated rats with hyperandrogenic state but not in those with hypoandrogenic state. 32 The 12.1DMT1 mice carry a genomic alteration targeted at an intergenic region adjacent to Grin2a. The genomic modification includes an insertion of a transgene cassette expressing MT1 under probasin promoter and a concomitant deletion of a B12.1-kb genomic region.…”

Section: Wtmentioning

confidence: 99%

Increased susceptibility of estrogen-induced bladder outlet obstruction in a novel mouse model

Tam

Zhang

Xiao

et al. 2015

Laboratory Investigation

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Disorders of the prostate and lower urinary tract are common in elderly men. We investigated the role of metallothionein-1 (MT1) in prostate carcinogenesis by generating a prostate-specific, MT1-expressing mouse. Unexpectedly, genomic analyses revealed that a 12.1-kb genomic region harboring several conserved noncoding elements was unintentionally deleted, upstream of the transgene integration site in the mouse, which we named it 12.1DMT1. Male 12.1DMT1 mice chronically treated with testosterone (T) plus 17b-estradiol (E2) to induce prostate cancer exhibited no evidence of precancerous or cancerous lesions. Instead, most of them exhibited a bladder outlet obstruction (BOO) phenotype not observed in treated wild-type (WT) mice. Thus, we hypothesized that 12.1DMT1 is a novel model for studying the hormonal requirement for BOO induction. Adult male 12.1DMT1 and WT mice were treated with T, E2, bisphenol A (BPA), T þ E2, or T þ BPA for up to 6 months. Histologic and immunohistochemical analysis of the prostate, bladder, and urethra were performed. No significant prostate pathologies were observed in WT or 12.1DMT1 mice treated with any of the hormone regimens. As expected, prostatic regression occurred in all E2-treated animals (WT and 12.1DMT1). Of great interest, despite a small prostate, 100% of E2-treated 12.1DMT1 mice, but only 40% of E2-treated WT mice, developed severe BOO (Po0.01). In contrast, T þ E2 treatment was less effective than E2 treatment in inducing severe BOO in 12.1DMT1 mice (68%, Po0.05) and was completely ineffective in WT animals. Similarly, T, BPA, and T þ BPA treatments did not induce BOO in either WT or 12.1DMT1 mice. The BOO pathology includes a thinner detrusor wall, narrowing of bladder neck and urethral lumen, and basal cell hyperplasia in the bladder body and urethra. These findings indicate that 12.1DMT1 mice exhibit enhanced susceptibility to E2-induced BOO that is independent of prostate enlargement but that is attenuated by the conjoint treatment with T. (2015) 95, 546-560; doi:10.1038/labinvest.2015 published online 23 February 2015 Bladder outlet obstruction (BOO) is regarded as a major cause of bothersome lower urinary tract symptoms (LUTS) in men. LUTS encompass a range of urinary morbidities, including those of storage, voiding, and postmicturition. 1 The incidence and prevalence of LUTS increase with age. 2 The etiologies of LUTS are multifactorial, and the pathophysiology is not well understood. 1,3 LUTS has often been attributed to benign prostatic hyperplasia (BPH), which narrows the urethral lumen and ultimately leads to BOO. However, a number of studies have suggested that BOO is not always caused by BPH. [4][5][6] Factors or organs other than the prostate have been proposed as contributors to BOO or modifiers of the severity of its symptoms. 3,7 An imbalance between androgens and estrogens has been implicated in the development of LUTS in men, including BOO. Higher levels of circulating 17b-estradiol (E2) were associated with an increased risk of LUTS in older men,...

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Prostatic inflammation and obstructive voiding in the adult noble rat: Impact of the testosterone to estradiol ratio in serum

Cited by 54 publications

References 33 publications

Hormone concentration, metabolic disorders and immunoexpression of androgen and estrogen-alpha receptors in men with benign prostatic hyperplasia and testosterone deficiency syndrome

Hormone concentration, metabolic disorders and immunoexpression of androgen and estrogen-alpha receptors in men with benign prostatic hyperplasia and testosterone deficiency syndrome

Hyperestrogenism and low serum testosterone-17β-estradiol ratio are associated with non-bacterial male accessory gland inflammation

Increased susceptibility of estrogen-induced bladder outlet obstruction in a novel mouse model

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