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Physical resistance training-induced changes in lipids metabolism pathways and apoptosis in prostate.
Lipids in Health and Disease ( IF 4.5 ) Pub Date : 2020-01-29 , DOI: 10.1186/s12944-020-1195-0
Giovana Rampazzo Teixeira 1, 2, 3 , Leonardo Oliveira Mendes 4 , Allice Santos Cruz Veras 2 , Hayley Hope Allyssa Thorpe 5 , Wagner José Fávaro 6 , Luiz Gustavo de Almeida Chuffa 7 , Patrícia Fernanda Felipe Pinheiro 7 , Francisco Eduardo Martinez 7
Affiliation  

BACKGROUND Altered lipid metabolism is an important characteristic of neoplastic cells, with androgens and growth factors being major regulatory agents of the lipid metabolism process. We investigated the effect of physical resistance training on lipid metabolism and apoptosis in the adult Wistar rat prostate. METHODS Two experimental groups represented sedentary and physical resistance training. Three days per week for 13 weeks, rats performed jumps in water carrying a weight load strapped to their chests as part of a physical resistance exercise protocol. Two days after the last training session, rats were anesthetized and sacrificed for blood and prostate analysis. RESULTS Physical exercise improved feeding efficiency, decreased weight gain, regulated the serum-lipid profile, and modulated insulin-like growth factor-1 (IGF-1) and free testosterone concentration. Furthermore, upregulation of cluster of differentiation 36 (CD36), sterol regulatory element binding protein-1 (SREBP-1), sterol regulatory element-binding protein cleavage-activating protein (SCAP), and reduced lysosome membrane protein (LIMPII) expression were also observed in the blood and prostates of trained rats. Consistent with these results, caspase-3 expression was upregulating and the BCL-2/Bax index ratio was decreased in trained rats relative to sedentary animals. CONCLUSIONS In this work, physical resistance training can alter lipid metabolism and increase markers of apoptosis in the prostate, suggesting physical resistance training as a potential novel therapeutic strategy for treating prostate cancer.

中文翻译:

体能训练引起的脂质代谢途径变化和前列腺细胞凋亡。

背景技术脂代谢的改变是赘生性细胞的重要特征,其中雄激素和生长因子是脂代谢过程的主要调节剂。我们调查了体力训练对成年Wistar大鼠前列腺脂质代谢和细胞凋亡的影响。方法两个实验组代表久坐和身体抵抗训练。每周三天,共13周,这是大鼠进行水上跳跃的运动,负重是绑在胸口的,这是体育锻炼的一部分。在最后一次训练后两天,麻醉大鼠并处死以进行血液和前列腺分析。结果体育锻炼提高了进食效率,减少了体重增加,调节了血脂水平,并调节胰岛素样生长因子-1(IGF-1)和游离睾丸激素的浓度。此外,分化簇36(CD36),固醇调节元件结合蛋白-1(SREBP-1),固醇调节元件结合蛋白裂解激活蛋白(SCAP)和溶酶体膜蛋白(LIMPII)表达降低也被上调。在训练大鼠的血液和前列腺中观察到。与这些结果一致,相对于久坐的动物,受过训练的大鼠中的caspase-3表达上调,BCL-2 / Bax指数比降低。结论在这项工作中,物理抵抗力训练可以改变脂质代谢并增加前列腺中凋亡的标志物,表明物理抵抗力训练是治疗前列腺癌的一种潜在的新型治疗策略。还观察到分化簇36(CD36)的上调,固醇调节因子结合蛋白1(SREBP-1),固醇调节因子结合蛋白裂解激活蛋白(SCAP)和溶酶体膜蛋白(LIMPII)表达降低。受过训练的大鼠的血液和前列腺。与这些结果一致,相对于久坐的动物,受过训练的大鼠中的caspase-3表达上调,BCL-2 / Bax指数比降低。结论在这项工作中,物理抵抗力训练可以改变脂质代谢并增加前列腺中凋亡的标志物,表明物理抵抗力训练是治疗前列腺癌的一种潜在的新型治疗策略。还观察到分化簇36(CD36)的上调,固醇调节因子结合蛋白1(SREBP-1),固醇调节因子结合蛋白裂解激活蛋白(SCAP)和溶酶体膜蛋白(LIMPII)表达降低。受过训练的大鼠的血液和前列腺。与这些结果一致,相对于久坐的动物,受过训练的大鼠中的caspase-3表达上调,BCL-2 / Bax指数比降低。结论在这项工作中,物理抵抗力训练可以改变脂质代谢并增加前列腺中凋亡的标志物,表明物理抵抗力训练是治疗前列腺癌的一种潜在的新型治疗策略。在受训大鼠的血液和前列腺中还观察到固醇调节元件结合蛋白裂解激活蛋白(SCAP)和溶酶体膜蛋白(LIMPII)表达降低。与这些结果一致,相对于久坐的动物,受过训练的大鼠中的caspase-3表达上调,BCL-2 / Bax指数比降低。结论在这项工作中,物理抵抗力训练可以改变脂质代谢并增加前列腺中凋亡的标志物,表明物理抵抗力训练是治疗前列腺癌的一种潜在的新型治疗策略。在受训大鼠的血液和前列腺中还观察到固醇调节元件结合蛋白裂解激活蛋白(SCAP)和溶酶体膜蛋白(LIMPII)表达降低。与这些结果一致,相对于久坐的动物,受过训练的大鼠中的caspase-3表达上调,BCL-2 / Bax指数比降低。结论在这项工作中,物理抵抗力训练可以改变脂质代谢并增加前列腺中凋亡的标志物,表明物理抵抗力训练是治疗前列腺癌的一种潜在的新型治疗策略。相对于久坐的动物,受过训练的大鼠中半胱氨酸天冬氨酸蛋白酶3表达上调并且BCL-2 / Bax指数比率降低。结论在这项工作中,物理抵抗力训练可以改变脂质代谢并增加前列腺中凋亡的标志物,表明物理抵抗力训练是治疗前列腺癌的一种潜在的新型治疗策略。相对于久坐的动物,受过训练的大鼠中半胱氨酸天冬氨酸蛋白酶3表达上调并且BCL-2 / Bax指数比率降低。结论在这项工作中,物理抵抗力训练可以改变脂质代谢并增加前列腺中凋亡的标志物,表明物理抵抗力训练是治疗前列腺癌的一种潜在的新型治疗策略。
更新日期:2020-01-30
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