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首页> 外文期刊>The FASEB Journal >Maternal folate depletion and high-fat feeding from weaning affects DNA methylation and DNA repair in brain of adult offspring
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Maternal folate depletion and high-fat feeding from weaning affects DNA methylation and DNA repair in brain of adult offspring

机译：来自断奶的母体叶酸耗尽和高脂肪饲料会影响成人后代脑中的DNA甲基化和DNA修复

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The mechanisms through which environmental and dietary factors modulate DNA repair are still unclear but may include dysregulation of gene expression due to altered epigenetic markings. In a mouse model, we investigated the effect of maternal folate depletion during pregnancy and lactation, and high-fat feeding from weaning, on base excision repair (BER) and DNA methylation and expression of selected BER-related genes in the brain of adult offspring. While folate depletion did not affect BER activity of the mothers, BER increased in the offspring at weaning (P=0.052). In the long term, as observed in 6-mo-old offspring, the double insult, i.e., maternal low-folate supply and high-fat feeding from weaning, decreased BER activity significantly in the cortex, cerebellum, hippocampus, and subcortical regions (P≤0.017). This fall in BER activity was associated with small changes in methylation or expression of BER-related genes. Maternal folate depletion led to slightly increased oxidative DNA damage levels in subcortical regions of adult offspring, which may increase sensitivity to oxidative stress and predispose to neurological disorders. In summary, our data suggest that low-folate supply during early life may leave an epigenetic mark that can predispose the offspring to further dietary insults, causing adverse effects during adult life.—Langie, S. A. S., Achterfeldt, S., Gorniak, J. P., Halley-Hogg, K. J. A., Oxley, D., van Schooten, F. J., Godschalk, R. W. L., McKay, J. A., Mathers, J. C. Maternal folate depletion and high-fat feeding from weaning affects DNA methylation and DNA repair in brain of adult offspring.
机译：环境和饮食因素调节DNA修复的机制仍然不清楚，但可能包括由于改变的表观遗传标记引起的基因表达的失调。在小鼠模型中，我们研究了孕妇叶酸耗尽在妊娠和哺乳期间的影响，以及断奶的高脂肪饲料，基础切除修复（BER）和DNA甲基化和成人后代大脑中所选BER相关基因的表达。虽然叶酸枯竭没有影响母亲的BER活动，但在断奶的后代增加（P = 0.052）。从长远来看，如6-Mo-Laving后代所观察到，双重损伤，即母体低叶酸供应和断奶的高脂肪，在皮质，小脑，海马和皮质区域中显着降低了BER活性（ p≤0.017）。这种落入BER活性与BER相关基因的甲基化或表达的小变化有关。母体叶酸耗尽导致成人后代的皮质区域略微增加氧化DNA损伤水平，这可能会增加对氧化应激的敏感性和易于神经障碍。总之，我们的数据表明，早期生命期间的低叶酸供应可能会留下一个表观遗传标记，可以使后代进一步饮食侮辱，导致成人寿命期间的不利影响。 - Langie，SAS，Achterfeldt，S。，Gorniak，JP，哈雷 - 霍格，KJA，OXLEY，D.，VAN SCHOOTEN，FJ，FJ，GODSCHALK，RWL，McKay，JA，MATHERS，JC母亲叶酸耗尽和来自断奶的高脂肪饲料会影响成人后代脑中的DNA甲基化和DNA修复。

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