Departament of Biological Sciences, São Paulo State University (UNESP), Institute of Biosciences, Humanities and Exact Sciences, São José do Rio Preto, São Paulo, Brazil.
Institute of Biomedical Sciences. Federal University of Uberlandia, Uberlândia, Minas Gerais, Brazil.
Reprod Biol. 2022 Sep;22(3):100674. doi: 10.1016/j.repbio.2022.100674. Epub 2022 Jul 25.
We examined the consequences of high-fat diet (HFD) on prostate histophysiology in two periods along sexual maturation of rats and the impact on the gland in adulthood. After weaning, male Wistar rats were fed a balanced diet (4 % fat-C3, C6, C9) or a HFD (20 % fat- HF3, HF6, HF9) for 3, 6 or 9 weeks. Fat deposit weights, blood glucose and levels of serum testosterone and estrogen were measured. Prostate was evaluated for histology, proliferative and apoptotic cell index, and for the expression of androgen (AR), estrogen receptors type α (ERα) and aromatase. HFD did not affect estrogen levels and elevated serum testosterone only in HF9. HFD reduced prostate weight in HF6 and increased it in adulthood (HF9) but relative prostate weight was unchanged among groups. Cell proliferation, height and density were higher in epithelium of all HFD-groups, compared to controls, featuring the epithelial hyperplasia. Epithelial apoptosis was lower in HF9. HF3 and HF9 exhibited higher expressions of ERα, indicating that HFD triggers a new activation of ERα expression in the acinar epithelium. The content of prostatic aromatase was also elevated in HF9. Increased numbers of AR-positive cells were observed in all HFD groups, and western blotting analysis showed an increase in the truncated form of 45 kDa (AR45) and a reduction in the expression of 110 kDa-AR for HF3 and HF9. In conclusion, excessive dietary fats during sexual maturation of rats led to developmental programming of the prostate, inducing a hyperplastic status with perturbations in AR isoforms expression and reactivation of ERα in adulthood, whose implications for posterior prostatic health could be detrimental.
我们研究了高脂肪饮食（HFD）在大鼠性成熟的两个阶段对前列腺组织生理学的影响，以及对成年期前列腺的影响。断奶后，雄性 Wistar 大鼠分别喂食平衡饮食（4%脂肪-C3、C6、C9）或高脂肪饮食（20%脂肪-HF3、HF6、HF9）3、6 或 9 周。测量脂肪沉积重量、血糖以及血清睾酮和雌激素水平。评估前列腺的组织学、增殖和凋亡细胞指数，以及雄激素（AR）、雌激素受体 α（ERα）和芳香酶的表达。HFD 不影响雌激素水平，仅在 HF9 中升高血清睾酮。HFD 在 HF6 中降低前列腺重量，并在成年期（HF9）增加，但各组之间的相对前列腺重量没有变化。与对照组相比，所有 HFD 组的上皮细胞增殖、高度和密度均增加，表现为上皮细胞增生。HF9 中的上皮细胞凋亡较低。HF3 和 HF9 表现出更高的 ERα 表达，表明 HFD 触发了腺上皮中 ERα 表达的新激活。HF9 中的前列腺芳香酶含量也升高。在所有 HFD 组中观察到更多的 AR 阳性细胞，Western blot 分析显示 45 kDa（AR45）截断形式增加，而 HF3 和 HF9 的 110 kDa-AR 表达减少。总之，大鼠性成熟期间过量的膳食脂肪导致前列腺发育编程，导致增生状态，AR 同工型表达出现波动，并在成年期重新激活 ERα，这可能对前列腺健康产生不利影响。
