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Parental diet, pregnancy outcomes and offspring health:metabolic determinants in developing oocytes and embryos

机译:父母的饮食,妊娠结局和后代的健康:卵母细胞和胚胎发育中的代谢决定因素

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摘要

The periconceptional period, embracing the terminal stages of oocyte growth and post-fertilisation development up to implantation, is sensitive to parental nutrition. Deficiencies or excesses in a range of macro- and micronutrients during this period can lead to impairments in fertility, fetal development and long-term offspring health. Obesity and genotype-related differences in regional adiposity are associated with impaired liver function and insulin resistance, and contribute to fatty acid-mediated impairments in sperm viability and oocyte and embryo quality, all of which are associated with endoplasmic reticulum stress and compromised fertility. Disturbances to maternal protein metabolism can elevate ammonium concentrations in reproductive tissues and disturb embryo and fetal development. Associated with this are disturbances to one-carbon metabolism, which can lead to epigenetic modifications to DNA and associated proteins in offspring that are both insulin resistant and hypertensive. Many enzymes involved in epigenetic gene regulation use metabolic cosubstrates (e.g. acetyl CoA and S-adenosyl methionine) to modify DNA and associated proteins, and so act as 'metabolic sensors' providing a link between parental nutritional status and gene regulation. Separate to their genomic contribution, spermatozoa can also influence embryo development via direct interactions with the egg and by seminal plasma components that act on oviductal and uterine tissues.
机译:围产期,包括卵母细胞生长和受精后发育直至植入的最终阶段,对父母的营养很敏感。在此期间,大量和微量营养素的缺乏或过量会导致生育能力,胎儿发育和长期后代健康受损。肥胖与基因型相关的区域性肥胖差异与肝功能受损和胰岛素抵抗有关,并导致脂肪酸介导的精子活力,卵母细胞和胚胎质量的损害,所有这些都与内质网应激和生育能力受损有关。对母体蛋白质代谢的干扰会提高生殖组织中铵的浓度,并干扰胚胎和胎儿的发育。与之相关的是对一碳代谢的干扰,这会导致后代中的DNA和相关蛋白的表观遗传修饰,这些修饰既具有胰岛素抵抗性又具有高血压性。表观遗传基因调控中涉及的许多酶都使用代谢共底物(例如乙酰辅酶A和S-腺苷甲硫氨酸)来修饰DNA和相关蛋白,因此可以充当``代谢传感器'',为父母的营养状况和基因调控之间提供联系。除了它们的基因组贡献外,精子还可以通过与卵的直接相互作用以及作用于输卵管和子宫组织的精浆成分来影响胚胎的发育。

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