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首页> 外文期刊>Cell and Tissue Research >High fat-induced obesity associated with insulin-resistance increases FGF-2 content and causes stromal hyperplasia in rat ventral prostate
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High fat-induced obesity associated with insulin-resistance increases FGF-2 content and causes stromal hyperplasia in rat ventral prostate

机译：高脂诱导的肥胖症与胰岛素抵抗相关，可增加FGF-2含量并引起大鼠腹侧前列腺间质增生

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Obesity affects sex hormone secretion, which can negatively influence prostatic structure, homeostasis, and disease. This investigation aimed to evaluate the repercussions of obesity induced by a high-fat diet on the rat prostate, with or without treatment with the aromatase inhibitor, Letrozole. Adult Wistar rats were fed a high-fat diet (20% saturated fat, O) for 15 weeks to induce obesity or received a balanced diet (4% fat, C). Then, a group of C and O rats were daily treated with Letrozole (1 mg/kg b.w. per day) for 2 weeks (CL and OL, respectively). Subsequently, ventral prostate was processed for analysis by transmission electron microscopy, immunohistochemistry, and Western blotting. Obesity decreased 70% of the testosterone plasma level. The prostate showed epithelial atrophy and dilated acini in the intermediate portion and epithelial wrinkling in the distal tips. The relative frequency of smooth muscle α-actin in the O group increased by 67%. Ultrastructurally, epithelial cells in obese animals presented altered secretory organelles, lipid droplets, and thicker subjacent fibromuscular layer. Letrozole treatment caused a partial restoration of the prostatic changes caused by obesity. Obesity increased the prostatic content of fibroblast growth factor-2 (FGF-2) by 150%, and Letrozole treatment increased this protein even more in the control and obese groups. This investigation shows that obesity provokes structural and ultrastructural changes in the epithelium of rat prostate; these changes might affect gland homeostasis and physiology. The epithelial and smooth muscle cell hyperplasia and increased FGF-2 expression observed in this experimental model of obesity/insulin-resistance might explain the high frequency of benign prostatic hyperplasia in insulin-resistant men.
机译：肥胖会影响性激素的分泌，这会对前列腺的结构，体内稳态和疾病产生负面影响。这项研究旨在评估高脂饮食对大鼠前列腺的肥胖影响，不论是否使用芳香酶抑制剂来曲唑治疗。给成年Wistar大鼠喂高脂饮食（20％饱和脂肪，O）15周，以诱导肥胖或接受均衡饮食（4％脂肪，C）。然后，每天给一组C和O大鼠用来曲唑治疗（每天1 mg / kg b.w.），持续2周（分别为CL和OL）。随后，对腹侧前列腺进行处理，以通过透射电子显微镜，免疫组织化学和蛋白质印迹进行分析。肥胖降低了睾丸激素血浆水平的70％。前列腺在中部显示上皮萎缩和扩张的腺泡，在远端顶端上皮起皱。 O组中平滑肌α-肌动蛋白的相对频率增加了67％。在肥胖动物中，超微结构上皮细胞的分泌细胞器，脂质滴和下层较厚的纤维肌层都有改变。来曲唑的治疗引起了由肥胖引起的前列腺改变的部分恢复。肥胖使成纤维细胞生长因子2（FGF-2）的前列腺含量增加了150％，来曲唑治疗在对照组和肥胖组中使该蛋白的含量更高。这项研究表明，肥胖症会引起大鼠前列腺上皮的结构和超微结构变化。这些变化可能会影响腺体的稳态和生理。在该肥胖/胰岛素抵抗实验模型中观察到的上皮和平滑肌细胞增生以及FGF-2表达增加可能解释了胰岛素抵抗男性中良性前列腺增生的高频率。

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