PDF(Pubmed)
Abstract：
Fetal brain development requires increased maternal protein intake to ensure that offspring reach their optimal cognitive potential in infancy and adulthood. While protein deficiency remains a prevalent issue in developing countries, it is also reemerging in Western societies due to the growing adoption of plant-based diets, some of which are monotonous and may fail to provide sufficient amino acids crucial for the brain\'s critical developmental phase. Confounding variables in human nutritional research have impeded our understanding of the precise impact of protein deficiency on fetal neurodevelopment, as well as its implications for childhood neurocognitive performance. Moreover, it remains unclear whether such deficiency could predispose to mental health problems in adulthood, mirroring observations in individuals exposed to prenatal famine. In this review, we sought to evaluate mechanistic data derived from rodent models, placing special emphasis on the involvement of neuroendocrine axes, the influence of sex and timing, epigenetic modifications, and cellular metabolism. Despite notable progress, critical knowledge gaps remain, including understanding the long-term reversibility of effects due to fetal protein restriction and the interplay between genetic predisposition and environmental factors. Enhancing our understanding of the precise mechanisms that connect prenatal nutrition to brain development in future research endeavors can be significantly advanced by integrating multiomics approaches and utilizing additional alternative models such as nonhuman primates. Furthermore, it is crucial to investigate potential interventions aimed at alleviating adverse outcomes. Ultimately, this research has profound implications for guiding public health strategies aimed at raising awareness about the crucial role of optimal maternal nutrition in supporting fetal neurodevelopment.
The Developmental Origins of Health and Disease theory posits that suboptimal conditions during early life exert a profound influence on adult health, potentially predisposing individuals to conditions such as neuropsychiatric disorders. By reviewing studies in rodents, we identified common mechanisms of how inadequate fetal protein uptake alters brain development and may contribute to anxiety, impaired memory function, and altered metabolism in adulthood. Adequate protein consumption during pregnancy is therefore critical to support healthy brain development.
The Developmental Origins of Health and Disease theory posits that suboptimal conditions during early life exert a profound influence on adult health, potentially predisposing individuals to conditions such as neuropsychiatric disorders. By reviewing studies in rodents, we identified common mechanisms of how inadequate fetal protein uptake alters brain development and may contribute to anxiety, impaired memory function, and altered metabolism in adulthood. Adequate protein consumption during pregnancy is therefore critical to support healthy brain development.
摘要：
胎儿大脑发育需要增加母体蛋白质的摄入量，以确保后代在婴儿期和成年期达到最佳的认知潜力。虽然蛋白质缺乏在发展中国家仍然是一个普遍的问题，由于越来越多地采用植物性饮食，它也在西方社会重新出现，其中一些是单调的，可能无法提供足够的氨基酸，对大脑的关键发育阶段至关重要。人类营养研究中的混杂变量阻碍了我们对蛋白质缺乏对胎儿神经发育的精确影响的理解。以及它对儿童神经认知能力的影响。此外，目前尚不清楚这种缺陷是否会导致成年后的心理健康问题，反映暴露于产前饥荒的个体的观察结果。在这次审查中,我们试图评估来自啮齿动物模型的机械数据，特别强调神经内分泌轴的参与，性别和时间的影响，表观遗传修饰,和细胞代谢。尽管取得了显著进展,关键的知识差距仍然存在，包括了解胎儿蛋白限制效应的长期可逆性以及遗传易感性和环境因素之间的相互作用。通过整合多组学方法并利用其他替代模型（例如非人灵长类动物），可以显着提高我们对将产前营养与未来研究工作中大脑发育联系起来的精确机制的理解。此外，研究旨在减轻不良结局的潜在干预措施至关重要.最终,这项研究对于指导旨在提高对母体最佳营养在支持胎儿神经发育中的关键作用的认识的公共卫生策略具有深远意义.
健康与疾病的发展起源理论认为，生命早期的次优条件对成人健康产生深远的影响。潜在的易感个体的条件，如神经精神疾病。通过回顾啮齿动物的研究，我们确定了胎儿蛋白质摄取不足如何改变大脑发育并可能导致焦虑的共同机制。记忆功能受损，并改变了成年后的新陈代谢。因此，怀孕期间充足的蛋白质消耗对于支持健康的大脑发育至关重要。
健康与疾病的发展起源理论认为，生命早期的次优条件对成人健康产生深远的影响。潜在的易感个体的条件，如神经精神疾病。通过回顾啮齿动物的研究，我们确定了胎儿蛋白质摄取不足如何改变大脑发育并可能导致焦虑的共同机制。记忆功能受损，并改变了成年后的新陈代谢。因此，怀孕期间充足的蛋白质消耗对于支持健康的大脑发育至关重要。
