Maternal High-Fat Diet Reduces Type-2 Neural Stem Cells and Promotes Premature Neuronal Differentiation during Early Postnatal Development.

Maternal High-Fat Diet Reduces Type-2 Neural Stem Cells and Promotes Premature Neuronal Differentiation during Early Postnatal Development.
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母亲高脂肪饮食会减少 2 型神经干细胞并促进产后早期发育过程中神经元的过早分化

DOI:
10.3390/nu14142813
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发表时间:
2022-07-08
期刊:
影响因子:
5.9
通讯作者:
--
中科院分区:
医学2区
文献类型:
--
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母亲肥胖或暴露于高脂肪饮食(HFD)对后代大脑的结构和功能发育具有不可逆转的影响。本研究旨在探讨妊娠和哺乳期母体HFD是否通过改变神经干细胞(NSCs)行为而损害后代齿状回(DG)神经发生。妊娠期和哺乳期分别饲喂鼠粮(CHD)和HFD(60%脂肪)。在出生后第1天(PND 1)、PND 10和PND 21采集幼犬。分析后代体重、脑结构和海马颗粒细胞层(GCL)厚度的变化。采用Nestin、Ki67、SOX2、Doublecortin (DCX)和NeuN免疫组化染色,观察海马NSCs在增殖和分化方面的行为。母体HFD加速了后代出生后的体重增加和大脑结构发育。它还减少了NSCs的数量及其增殖,导致NSCs池大小减小。此外,在出生后早期发育阶段,母体HFD加剧了NSCs的消耗并促进了神经元分化。这些发现表明,在出生后海马发育过程中,母体HFD摄入通过减少2型NSCs和促进过早神经元分化,显著降低了NSCs的数量和能力。
Maternal obesity or exposure to a high-fat diet (HFD) has an irreversible impact on the structural and functional development of offspring brains. This study aimed to investigate whether maternal HFD during pregnancy and lactation impairs dentate gyrus (DG) neurogenesis in offspring by altering neural stem cells (NSCs) behaviors. Pregnant Sprague-Dawley rats were fed a chow diet (CHD) or HFD (60% fat) during gestation and lactation. Pups were collected on postnatal day 1 (PND 1), PND 10 and PND 21. Changes in offspring body weight, brain structure and granular cell layer (GCL) thickness in the hippocampus were analyzed. Hippocampal NSCs behaviors, in terms of proliferation and differentiation, were investigated after immunohistochemical staining with Nestin, Ki67, SOX2, Doublecortin (DCX) and NeuN. Maternal HFD accelerated body weight gain and brain structural development in offspring after birth. It also reduced the number of NSCs and their proliferation, leading to a decrease in NSCs pool size. Furthermore, maternal HFD intensified NSCs depletion and promoted neuronal differentiation in the early postnatal development period. These findings suggest that maternal HFD intake significantly reduced the amount and capability of NSCs via reducing type–2 NSCs and promoting premature neuronal differentiation during postnatal hippocampal development.