As two most common progressive diseases of aging, type 2 diabetes mellitus (T2DM) and benign prostatic hyperplasia (BPH) were all characterized by endocrine and metabolic disorders. Here, our clinical study showed that there were significant differences in fasting blood glucose (FBG), fasting insulin (FINS), insulin resistance index (HOMA-IR) and prostate volume (PV) between simple BPH patients and BPH complicated with T2DM patients. Further analysis showed that HOMA-IR was positively correlated with PV in BPH complicated with T2DM patients. The in vitro experiment results showed that high glucose (HG) promoted EMT process in a glucose-dependent manner in human prostate hyperplasia cells (BPH-1) and prostate cancer cells (PC-3), and this pathological process was exacerbated by co-culture with insulin. Mechanistically, insulin-induced exacerbation of EMT was depended on the activation of MEK/ERK signaling pathway, and we suggested that insulin and its analogs should be used very carefully for the clinical antihyperglycemic treatment of BPH complicated with T2DM patients.

2 型糖尿病 (T2DM) 和良性前列腺增生 (BPH) 作为两种最常见的进行性衰老疾病，均以内分泌和代谢紊乱为特征。在这里，我们的临床研究表明，单纯性 BPH 患者与 BPH 合并 T2DM 患者的空腹血糖 (FBG)、空腹胰岛素 (FINS)、胰岛素抵抗指数 (HOMA-IR) 和前列腺体积 (PV) 存在显着差异。进一步分析表明，在 BPH 合并 T2DM 患者中，HOMA-IR 与 PV 呈正相关。在体外实验结果表明，高糖（HG）以葡萄糖依赖性方式促进人前列腺增生细胞（BPH-1）和前列腺癌细胞（PC-3）的EMT过程，与胰岛素共培养加剧了这种病理过程. 从机制上讲，胰岛素诱导的 EMT 恶化取决于 MEK/ERK 信号通路的激活，我们建议胰岛素及其类似物应非常谨慎地用于 BPH 合并 T2DM 患者的临床降糖治疗。