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

Shi Fu,Huan Xu,Qiong Wang,Zhikang Cai,Meng Gu,Xiang Wan,Chong Liu,Zhong Wang,Qi Chen,Juan Zhou,Yanbo Chen,Yubing Peng

doi:10.1038/srep43771

Abstract

The incidence of benign prostatic hyperplasia (BPH) is increasing among obese individuals, but few studies have fully explained the underlying mechanisms. We aimed to elucidate the relationship between obesity and BPH. Herein, we show that in prostatic epithelial and stromal cells, adiponectin exerts multifunctional effects including anti-proliferation, blocking of G1/S-phase progression and the promotion of apoptosis via inhibiting the MEK-ERK-p90RSK axis. Furthermore, we found that a high-fat diet (HFD) led to adiponectin deficiency and microscopic BPH in a mouse model of obesity. And an adiponectin supplement protected the obese mice from microscopic BPH. The present study provides evidence that adiponectin is a protective regulator in the development and progression of BPH and that adiponectin deficiency causally links BPH with obesity.

Highlights

Positive controls were skeletal muscle tissue extract for AdipoR1 and liver extract for AdipoR2
RWPE1 and WPMY1 cells had a larger extent of expression of AdipoR1 than of AdipoR2 at both the mRNA and protein levels (Fig. 1c,d), and AdipoR1 was abundantly expressed on the membrane of RWPE1 and WPMY1 cells (Fig. 1e)
To previous studies[24,36,37], we found that phosphorylation of MEK1/2, ERK1/2 and p90 ribosomal S6 kinase (p90RSK) induced by epidermal growth factor (EGF) or foetal bovine serum (FBS) was significantly attenuated by adiponectin treatment

Summary

Introduction

Positive controls were skeletal muscle tissue extract for AdipoR1 and liver extract for AdipoR2. The results were adjusted by GAPDH expression and quantitated as described in the Methods section (n = 3, Student’s t-test, **p < 0.01). AdipoR1 and AdipoR2 in RWPE1 and WPMY1 cells were determined by RT-PCR. The results were adjusted by β-actin and quantitated by the 2−ΔΔCt method (n = 3, Student’s t-test, **p < 0.01). (e) Immunofluorescence staining (green) for AdipoR1 and AdipoR2 in RWPE1 and WPMY1 cells, DAPI staining (blue) for nucleus. Are associated with an increased risk of BPH and prostate cancer[19,20]. These studies led us to hypothesize that adiponectin deficiency could be a potential pathogenic mechanism linking BPH with obesity. We established the emergence of microscopic BPH due to deficiency of adiponectin in an obesity mouse model

Objectives

Methods

Results

Conclusion