Pinto-Fochi Maria Etelvina, Pytlowanciv Eloísa Zanin, Reame Vanessa, Rafacho Alex, Ribeiro Daniele Lisboa, Taboga Sebastião Roberto, Góes Rejane Maira
Department of BiologyInstitute of Biosciences, Letters and Exact Sciences, Univ Estadual Paulista - IBILCE/UNESP, São José do Rio Preto, São Paulo, Brazil.
Department of Structural and Functional BiologyInstitute of Biology, State University of Campinas, IB/UNICAMP, Campinas, São Paulo, Brazil.
Reproduction. 2016 Dec;152(6):795-808. doi: 10.1530/REP-16-0072. Epub 2016 Sep 27.
This study evaluated the impact of a high-fat diet (HFD) during different stages of rat life, associated or not with maternal obesity, on the content of sex steroid hormones and morphophysiology of Leydig cells. The following periods of development were examined: gestation (O1), gestation and lactation (O2), from weaning to adulthood (O3), from lactation to adulthood (O4), gestation to adulthood (O5), and after sexual maturation (O6). The HFD contained 20% unsaturated fat, whereas the control diet had 4% fat. Maternal obesity was induced by feeding HFD 15 weeks before mating. All HFD groups presented increased body weight, hyperinsulinemia and reduced insulin sensitivity. Except for O1, all HFD groups exhibited a higher adiposity index, hyperleptinemia, reduced testosterone and estradiol testicular levels, and decreased testicular 17β-HSD enzyme . Morphometrical analyses indicated atrophy of Leydig cells in the O2 group. Myelin vesicles were observed in the mitochondrial matrix of Leydig cells in O3, O4, O5 and O6, and autophagosomes containing mitochondria were found in O5 and O6. In conclusion, HFD feeding, before or after sexual maturation, reduces the functional capacity of rat Leydig cells. Maternal obesity associated with HFD during pregnancy/lactation prejudices Leydig cell steroidogenesis and induces its atrophy in adulthood, even if it is replaced by a conventional diet at later stages of life. Regardless of the life period of exposure to HFD, deregulation of leptin is the main factor related to steroidogenic impairment of Leydig cells, and, in groups exposed for longer periods (O3, O4, O5 and O6), this is worsened by structural damage and mitochondrial degeneration of these cells.
本研究评估了大鼠生命不同阶段的高脂饮食（HFD），无论是否与母体肥胖相关，对性类固醇激素含量和睾丸间质细胞形态生理学的影响。研究考察了以下发育阶段：妊娠期（O1）、妊娠期和哺乳期（O2）、从断奶到成年期（O3）、从哺乳期到成年期（O4）、从妊娠期到成年期（O5）以及性成熟后（O6）。高脂饮食含有20%的不饱和脂肪，而对照饮食含有4%的脂肪。在交配前15周通过喂食高脂饮食诱导母体肥胖。所有高脂饮食组的体重均增加，出现高胰岛素血症且胰岛素敏感性降低。除O1组外，所有高脂饮食组的肥胖指数更高、瘦素血症、睾丸睾酮和雌二醇水平降低，以及睾丸17β - HSD酶活性降低。形态计量学分析表明O2组睾丸间质细胞萎缩。在O3、O4、O5和O6组的睾丸间质细胞线粒体基质中观察到髓鞘样小泡，在O5和O6组中发现含有线粒体的自噬体。总之，在性成熟前后喂食高脂饮食会降低大鼠睾丸间质细胞的功能能力。妊娠/哺乳期与高脂饮食相关的母体肥胖会损害睾丸间质细胞的类固醇生成，并在成年期诱导其萎缩，即使在生命后期改用常规饮食也是如此。无论暴露于高脂饮食的生命阶段如何，瘦素失调是与睾丸间质细胞类固醇生成受损相关的主要因素，并且在暴露时间较长的组（O3、O4、O5和O6）中，这些细胞的结构损伤和线粒体变性会使情况恶化。
