Xu Congyun, Xu Yan, Shen Zhou, Zhou Hangcheng, Xiao Jun, Huang Tao
Department of Urology, Anhui Provincial Hospital, The First Affiliated Hospital of University of Science and Technology of China, #17 Lujiang Road, Hefei, 230001, China.
Department of Pathology, Anhui Provincial Hospital, The First Affiliated Hospital of University of Science and Technology of China, #17 Lujiang Road, Hefei, 230001, China.
Int Urol Nephrol. 2018 Apr;50(4):611-617. doi: 10.1007/s11255-018-1826-9. Epub 2018 Feb 19.
To investigate the efficacy of insulin sensitizer on prostatic tissue in animal model with benign prostatic hyperplasia (BPH) secondary to metabolic syndrome (MetS).
Models were established by providing Sprague-Dawley rats with high fat diet (HFD) combined with metformin or not. All objects were killed 40 days later with prostatic tissue being removed, weighed before stained, as well as the expression level of insulin-like growth factor I (IGF-1) and receptor (IGF-1R) being measured, and the level of insulin resistance (IR) has also been evaluated.
Model has been successfully established. Level of prostatic hyperplasia and IR as well as IGF-1 and IGF-1R expressions in the blank and saline control subunits of HFD group was higher than that of normal diet group (P < 0.05). In the subunit of metformin, along with the suppression of IR, the level of prostatic hyperplasia and the expression of IGF-1 pathway have both decreased (P < 0.05).
MetS can promote the growth of prostate during the formation of central obesity and IR. IGF-1 pathway may have an important role in the induction of BPH following IR. The application of metformin can suppress the expression of IGF-1 and IGF-1R, thus preventing the promotive effect of IR on prostate tissue in animal model of MetS.
研究胰岛素增敏剂对继发于代谢综合征（MetS）的良性前列腺增生（BPH）动物模型前列腺组织的疗效。
通过给Sprague-Dawley大鼠喂食高脂饮食（HFD）并联合或不联合二甲双胍来建立模型。40天后处死所有实验对象，取出前列腺组织，称重并进行染色，同时检测胰岛素样生长因子I（IGF-1）及其受体（IGF-1R）的表达水平，并评估胰岛素抵抗（IR）水平。
模型成功建立。HFD组空白和生理盐水对照组的前列腺增生程度、IR水平以及IGF-1和IGF-1R表达均高于正常饮食组（P<0.05）。在二甲双胍组，随着IR的抑制，前列腺增生程度和IGF-1通路的表达均降低（P<0.05）。
MetS在中心性肥胖和IR形成过程中可促进前列腺生长。IGF-1通路可能在IR诱导的BPH中起重要作用。二甲双胍的应用可抑制IGF-1和IGF-1R的表达，从而在MetS动物模型中阻止IR对前列腺组织的促进作用。
