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Abstract
Benign prostatic hyperplasia (BPH) is a common disease in older men, and there is
evidence that obesity is a causal factor. It is currently unclear whether the hormone
leptin, which is positively correlated to obesity, is involved in BPH. The aim of
this study was to determine the effect of leptin on testosterone-induced BPH in mice
and to explore possible underlying mechanisms. Testosterone (3 mg/kg) was injected
into wild-type and leptin-deficient ob/ob male mice for 14 consecutive days, and prostate
tissues were subjected to various analyses. Additionally, BPH epithelial-1 (BPH-1)
cells were treated with leptin to further investigate the underlying mechanisms. Leptin
deficiency attenuated testosterone-induced morphological and pathological changes
of BPH in mice. Furthermore, leptin deficiency alleviated the process of epithelial-mesenchymal
transition (EMT) and suppressed the downregulation of bone morphogenic protein and
activin membrane-bound inhibitor (BAMBI) in testosterone-treated mice. The in vitro
data revealed that leptin significantly increased the expression of the EMT-associated
marker vimentin but decreased the expression of E-cadherin, and that upregulation
of BAMBI mitigated the intensity of leptin-induced EMT responses. Our results suggest
that leptin can promote EMT in BPH through downregulating BAMBI. Suppressing leptin
might be a potential therapeutic approach in preventing BPH development and progression.