Adiponectin deficiency contributes to the development and progression of benign prostatic hyperplasia in obesity

Fu, Shihui; Xu, Huan; Gu, Meng; Liu, Chong; Wang, Qiong; Wan, Xiang; Chen, Yan-Bo; Chen, Qi; Peng, Yue; Cai, Zhixiang; Zhou, Juan; Wang, Zhong

doi:10.1038/srep43771

Cited by 20 publications

(18 citation statements)

References 63 publications

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“…Although the exact role of ERK is yet to be revealed in BPH, Papatsoris and Papavassiliou (2001) suggested the action of MAPK signaling as one of the molecular bases of BPH. Some studies, including our previous report, show that ERK is regulated in the enlarged prostate ( Fu et al, 2017 ; Xu et al, 2017 ; Youn et al, 2017 ) or proliferation of prostate stromal cells ( Zhang et al, 2008 ; Youn et al, 2017 ). Other studies report that the ERK cascade is phosphorylated in reaction to AR, leading to cell cycle progression in prostate cancer ( Peterziel et al, 1999 ; Migliaccio et al, 2000 ).…”

Section: Introductionmentioning

confidence: 81%

“…Although several other studies also showed that the MAPK pathway is closely related to cell proliferation in prostate cancer ( Papatsoris et al, 2007 ; Rybak et al, 2015 ), the exact role of MAPK signaling pathway in BPH is yet to be cleared. Especially, ERK signaling is a considerable interest in BPH because our and other previous studies showed that the ERK signaling is activated in BPH conditions in vivo and in vitro ( Zhang et al, 2008 ; Fu et al, 2017 ; Xu et al, 2017 ; Youn et al, 2017 ). In consistent with such reports, our findings indicate that ERK is dramatically activated under BPH conditions and subsequently returned to normal levels by BBR treatment, but phosphorylation levels of JNK and p38 were not significantly affected in BPH-induced rats ( Figure 3 ).…”

Section: Discussionmentioning

confidence: 99%

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Berberine Improves Benign Prostatic Hyperplasia via Suppression of 5 Alpha Reductase and Extracellular Signal-Regulated Kinase in Vivo and in Vitro

et al. 2018

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Benign prostate hyperplasia (BPH) is a common disease in elderly men, characterized by proliferated prostate and urinary tract symptoms. The hormonal cascade starting by the action of 5-alpha-reductase (5AR) is known to be one of the pathways responsible for the pathogenesis of BPH. Present investigation evaluated the capacity of berberine (BBR), a nature-derived compound abundant in Coptis japonica, in testosterone-induced BPH rats. Experimental BPH was induced by inguinal injection with testosterone propionate (TP) for 4 weeks. BBR or finasteride, a 5AR inhibitor as positive control, was treated for 4 weeks during BPH. BPH induced by TP evoked weight gaining and histological changes of prostate and BBR treatment improved all the detrimental effects not only weight reduction and histological changes but also suppression of prostate-specific antigen (PSA), which is elevated during BPH. Additionally, BBR suppressed TP-associated increase of 5AR, androgen receptor (AR) and steroid coactivator-1 (SRC-1), the key factors in the pathogenesis of BPH. To evaluate the underlying molecular mechanisms responsible for beneficial effects of BBR, we investigated whether these effects were associated with the mitogen-activated protein kinase pathway. BPH induced by TP showed increased phosphorylation of extracellular signal-regulated kinase (ERK), whereas this was suppressed by BBR treatment. On the other hand, c-jun-N-terminal kinase (JNK) and p38 mitogen-activated protein kinase was not changed in BPH rats. In in vitro study using RWPE-1 cells, a human prostate epithelial cell line. TP increased cell proliferation and BPH-related key factors such as PSA, AR, and 5AR in RWPE-1 cells, and those factors were significantly decreased in the presence of BBR. Furthermore, these proliferative effects in RWPE-1cells were attenuated by treatment with U0126, an ERK inhibitor, confirming BBR can relieve overgrowth of prostate via ERK-dependent signaling. The cotreatment of U0126 and BBR did not affect the change of 5AR nor proliferation compared with U0126 alone, suggesting that the effect of BBR was dependent on the action of ERK. In conclusion, this study shows that BBR can be used as a therapeutic agent for BPH by controlling hyperplasia of prostate through suppression of ERK mechanism.

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Section: Introductionmentioning

confidence: 81%

Section: Discussionmentioning

confidence: 99%

Berberine Improves Benign Prostatic Hyperplasia via Suppression of 5 Alpha Reductase and Extracellular Signal-Regulated Kinase in Vivo and in Vitro

et al. 2018

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“…Previous studies on the association of BPH and adipokines (e.g., C-peptide, leptin and adiponectin) have reported conflicting results [6][7][8]. To the best of our knowledge, there are no reports of a relationship between omentin and BPH.…”

Section: Backgroudmentioning

confidence: 92%

Serum omentin-1 level in patients with benign prostatic hyperplasia

Hao

et al. 2020

BMC Urol

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Backgroud: To evaluate the relationship between omentin-1 and benign prostatic hyperplasia (BPH). BPH is the most common urological disease in elderly men worldwide. Lower serum omentin-1 levels were reported to be negatively associated with the incidence of inflammation, diabetes, obesity and metabolic syndrome, which all play a role in the development of BPH. To the best of our knowledge, the relationship between omentin-1 and BPH has not been investigated previously. Methods: A total of 70 males participated in this study, including forty patients diagnosed with BPH and thirty healthy males. The anthropometric measurements and the biochemical parameters were measured in this study. We evaluated serum omentin-1 levels and the correlation with those data. We also test the gene expression of IL-8, IL-18 in BPH group using the TURP tissues. Results: The serum omentin-1 levels were lower in the BPH patients than in the control group (27.95 ± 4.18 versus 32.03 ± 5.46, p < 0.001). The general characteristics and biochemical parameters were investigated, and a negative correlation was found between serum omentin-1 levels and BMI in the BPH group (r = − 0.391, p = 0.013) as well as the whole group (r = − 0.457, p < 0.001). Multiple-factor binary regression analysis revealed that serum omentin-1was a protective factor of BPH development. Furthermore, lower serum omentin-1 levels were associated with higher mRNA expression of IL-8 or IL-18 in the BPH group. Conclusion: Omentin-1 may suppress the development of BPH and Lower serum omentin-1 levels in BPH patients might associated with higher prostate volume and higher IL-8 and IL-18 expression levels in their prostatic cells.

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“…Adiponectin was also found to have anti-proliferation effects on prostatic cancer cells [111]. Adiponectin induces cell cycle arrest of prostatic epithelial and stromal cell lines and induces apoptosis by increasing caspase-3 and downregulating of Bcl2 (B cell lymphoma) gene [112].…”

Section: • Prostate Cancermentioning

confidence: 97%

Adipocytokines: Are they the Theory of Everything?

et al. 2020

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Introduction: Adipose tissue secretes various bioactive peptides/proteins, immune molecules and inflammatory mediators which are known as adipokines or adipocytokines. Adipokines play important roles in the maintenance of energy homeostasis, appetite, glucose and lipid metabolism, insulin sensitivity, angiogenesis, immunity and inflammation. Enormous number of studies from all over the world proved that adipocytokines are involved in the pathogenesis of diseases affecting nearly all body systems, which raises the question whether we can always blame adipocytokines as the triggering factor of every disease that may hit the body. Objective: Our review targeted the role played by adipocytokines in the pathogenesis of different diseases affecting different body systems including diabetes mellitus, kidney diseases, gynecological diseases, rheumatologic disorders, cancers, Alzheimer's, depression, muscle disorders, liver diseases, cardiovascular and lung diseases. Methodology: We cited more than 33 recent literature reviews that discussed the role played by adipocytokines in the pathogenesis of different diseases affecting different body systems. Conclusion: More evidence is being discovered to date about the role played by adipocytokines in more diseases and extra research is needed to explore hidden roles played by adipokine imbalance on disease pathogenesis.

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Adiponectin deficiency contributes to the development and progression of benign prostatic hyperplasia in obesity

Cited by 20 publications

References 63 publications

Berberine Improves Benign Prostatic Hyperplasia via Suppression of 5 Alpha Reductase and Extracellular Signal-Regulated Kinase in Vivo and in Vitro

Berberine Improves Benign Prostatic Hyperplasia via Suppression of 5 Alpha Reductase and Extracellular Signal-Regulated Kinase in Vivo and in Vitro

Serum omentin-1 level in patients with benign prostatic hyperplasia

Adipocytokines: Are they the Theory of Everything?

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