大鼠模型代际蛋白缺乏与雌性后代(F1和F2)青春期生殖功能的关系

IF 2.1 Q3 PHYSIOLOGY Current research in physiology Pub Date : 2022-01-01 DOI:10.1016/j.crphys.2021.12.003
Nosarieme O. Abey, Osaretin A.T. Ebuehi, Ngozi O.A. Imaga
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引用次数: 1

摘要

生殖功能不足是通过自然选择进化而来的一个重要特征。营养可以在不同程度上调节生殖活动,其对生殖的影响被认为是复杂的,难以预测的。目的探讨早期持续膳食蛋白质缺乏对后代(F1和F2)生殖参数的潜在影响。方法4组(4只)每日饲喂蛋白质饲粮(PD),按蛋白质饲粮的不同比例配制为:21%蛋白质饲粮、10%蛋白质饲粮、5%蛋白质饲粮和对照饲粮(含16-18%蛋白质的大鼠饲料)。它们在交配前、整个妊娠期和哺乳期都是自由喂养的,下一代断奶后继续吃母鼠的食物。生殖功能分析(包括;进行妊娠期和青春期激素分析、青春期开始、发情周期、性反应)和卵巢结构形态计量学分析,以评估相关后果。结果生育指数(对照;85.8%。pd, 21%;88.43%。,与10%PD相比;65.9%。pd, 5%;(35.78%),在F2中也分别出现,这是由于蛋白质缺陷模型的生殖功能改变造成的(P≤0.05)。低蛋白饮食导致子宫内状况不佳,这与产前发病率和死亡率增加有关(对照;11.3%。pd, 21%;3.3%。pd, 10%;27.4%。pd, 5%;32.9%),低出生体重(对照组;5.29, 4.9 g, 21%PD;5.5, 5.06 g, 10%PD;4.05, 3.86 g, 5%PD;2.7, 2.5 g),分别在F1和F2,青春期延迟(平均青春期年龄设为:对照;PND 36, 21%pd;PND为38,pd为10%;62年患产后抑郁症。, 5%PD;PND 67),其次是诱导周期不规则,卵泡成熟改变和内分泌功能障碍,5%PD更为严重。结论雌性生物的生殖状态取决于卵巢结构和功能的维持,而卵巢结构和功能的维持与下丘脑-垂体-性腺轴、激素事件和性成熟有关。因此,在生命早期持续的蛋白质缺乏和生殖反应之间存在关联,这在机械上涉及关键卵巢细胞结构和功能的终身变化。
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Intergenerational protein deficiency and adolescent reproductive function of subsequent female generations (F1 and F2) in rat model

Background

Efficient reproductive function is an important characteristic that has evolved through natural selection. Nutrition can modulate reproductive activities at different levels, and its effect on reproduction is deemed complex and less predictable.

Objective

This study aims at investigating the underlying effect of persistent dietary protein deficiency during early life on reproductive parameters of subsequent (F1 and F2) generations.

Method

Rats in group of four (4) were fed daily, different ration of protein diet (PD) formulated as: 21% protein diet, 10%protein diet, 5%protein diet and control diet (rat chow, containing 16–18% protein). They were fed ad libitum before mating, throughout gestation and lactation, and next generations were weaned to the maternal diet. Reproductive function analysis (which include; gestation and pubertal hormonal profiling, onset of puberty, oestrus cyclicity, sexual response) and morphometric analysis of the ovarian structure were carried out to assess associated consequences.

Results

There was significant reduction in the fertility index (Control; 85.8%., 21%PD; 88.43%., as compared to 10%PD; 65.9%., 5%PD; 35.78%.,) at F1, also recurring in F2 respectively as a consequence of altered reproductive function in the protein deficient models at P ≤ 0.05. Low protein diet posed suboptimal intrauterine condition, which was linked to increased prenatal morbidity and mortality (control; 11.3%., 21%PD; 3.3%., 10%PD; 27.4%., 5%PD; 32.9%), low birthweight (control; 5.29, 4.9 g., 21%PD; 5.5, 5.06 g., 10%PD; 4.05, 3.86 g., 5%PD; 2.7, 2.5 g) at F1 and F2 respectively, delayed onset of puberty (with average pubertal age set at: control; PND 36, 21%PD; PND 38 while 10%PD; PND 62., and 5%PD; PND 67), followed by induced cycle irregularity, altered follicular maturation and endocrine dysfunction, more severe in 5%PD.

Conclusion

Reproductive status of a female organism depends on the maintenance of ovarian structure and function that has been associated with the hypothalamic pituitary-gonadal axis, hormonal events and sexual maturity. There is therefore an association between persistent early life protein deficiency and reproductive response which mechanistically involves life-long changes in key ovarian cytoarchitecture and function.

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