PNAS:母亲饮食有多重要?“吃不对”对后代影响巨大……
2018/07/04
对孕妇来说,保证营养充足是最常被提醒的注意事项之一。近日,发表在PNAS上的一项新研究再次证实了孕期“合理饮食”的重要性。


图片来源:PNAS( https://doi.org/10.1073/pnas.1721876115)

在6月25日发表的题为“Mouse maternal protein restriction during preimplantation alone permanently alters brain neuron proportion and adult short-term memory”的研究中,来自英国南安普顿大学的科学家们证实,怀孕早期母亲饮食中蛋白质不足会对后代大脑发育产生持久的影响。

具体来说,由Sandrine Willaime-Morawek博士和Tom Fleming教授带领的团队首次证实,在小鼠怀孕的头些天(着床前期,pre-implantation period),母亲营养不良不仅对后代早期大脑发育不利,还会影响成年时的记忆。


图片来源:16sucai

众所周知,怀孕早期母亲的饮食对胎儿的发育至关重要,如果饮食不佳,会增加后代在以后生活中的患病(如心血管疾病、精神分裂症)风险。

事实上,先前已有研究表明,怀孕和哺乳期间母亲饮食中蛋白质减少会损害婴儿的大脑,对协调和认知功能产生持久的影响。但在着床前期母亲营养对大脑发育的重要性一直是未知的。


Neural stem cells making nerve cells during mouse development. Credit: University of Southampton

该研究中,利用细胞培养和小鼠模型,科学家们发现,在着床前期,母亲的低蛋白饮食会减少神经干细胞的产生,从而导致神经细胞形成的时机和数量发生错误,最终使得后代在成年时短期记忆较差。

Willaime-Morawek博士说:“我们的初步研究表明,在小鼠模型中,怀孕早期母亲营养不良会对大脑发育以及成年记忆产生不利影响。同时,我们也证实了着床前期是决定成年表型的关键。”

总结来说,这篇论文表明,仅在着床前期限制小鼠母亲饮食中的蛋白质就能永久性地改变大脑神经元比例以及成年时的短期记忆。

责编:风铃

参考资料:

Research reveals early maternal diet affects brain development and adult memory

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  • Mouse maternal protein restriction during preimplantation alone permanently alters brain neuron proportion and adult short-term memory

    Maternal protein malnutrition throughout pregnancy and lactation compromises brain development in late gestation and after birth, affecting structural, biochemical, and pathway dynamics with lasting consequences for motor and cognitive function. However, the importance of nutrition during the preimplantation period for brain development is unknown. We have previously shown that maternal low-protein diet (LPD) confined to the preimplantation period (Emb-LPD) in mice, with normal nutrition thereafter, is sufficient to induce cardiometabolic and locomotory behavioral abnormalities in adult offspring. Here, using a range of in vivo and in vitro techniques, we report that Emb-LPD and sustained LPD reduce neural stem cell (NSC) and progenitor cell numbers at E12.5, E14.5, and E17.5 through suppressed proliferation rates in both ganglionic eminences and cortex of the fetal brain. Moreover, Emb-LPD causes remaining NSCs to up-regulate the neuronal differentiation rate beyond control levels, whereas in LPD, apoptosis increases to possibly temper neuron formation. Furthermore, Emb-LPD adult offspring maintain the increase in neuron proportion in the cortex, display increased cortex thickness, and exhibit short-term memory deficit analyzed by the novel-object recognition assay. Last, we identify altered expression of fragile X family genes as a potential molecular mechanism for adverse programming of brain development. Collectively, these data demonstrate that poor maternal nutrition from conception is sufficient to cause abnormal brain development and adult memory loss.

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