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The effect of maternal high-fat/high-sugar diet on offspring oocytes and early embryo development

机译:母体高脂/高糖饮食对后代卵母细胞和早期胚胎发育的影响

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摘要

Observational human data and several lines of animal experimental data indicate that maternal obesity impairs offspring health. Here, we comprehensively tested the model that maternal obesity causes defects in the next three generations of oocytes and embryos. We exposed female F0 mice to a high-fat/high-sugar (HF/HS) diet for 6 weeks before conception until weaning. Sires, F1 offspring and all subsequent generations were fed control chow diet. Oocytes from F1, F2 and F3 offspring of obese mothers had lower mitochondrial mass and less ATP and citrate than oocytes from offspring of control mothers. F0 blastocysts from HF/HS-exposed mice, but not F1 and F2 blastocysts, had lower mitochondrial mass and membrane potential, less citrate and ATP and smaller total cell number than F0 blastocysts from control mothers. Finally, supplementation of IVF media with the anti-oxidant mito-esculetin partially prevented the oocyte mitochondrial effects caused by maternal HF/HS diet. Our results support the idea that maternal obesity impairs offspring oocyte quality and suggest that antioxidant supplementation should be tested as a means to improve IVF outcomes for obese women.
机译:观察人体数据和几种动物实验数据表明母体肥胖损害后代健康。在这里,我们全面测试了母体肥胖导致在接下来的三代卵母细胞和胚胎中的缺陷的模型。在概念之前,我们将雌性F0小鼠暴露于高脂/高糖(HF / HS)饮食中直至断奶。 F1后代和所有后续几代人的胎儿喂食控制饮食。来自F1,F2和F3的卵母细胞的肥胖母亲的后代具有较低的线粒体质量,少于ATP和柠檬酸盐而不是来自对照母亲的后代的卵母细胞。来自HF / HS暴露小鼠的F0胚泡,但不是F1和F2胚泡,具有较低的线粒体质量和膜电位,较少的柠檬酸盐和ATP和来自对照母亲的F0胚泡的较小总细胞数。最后,用抗氧化型Mito-Esculetin补充IVF培养基部分地阻止了母体HF / HS饮食引起的卵母细胞线粒体效应。我们的结果支持母体肥胖损害后代卵母细胞质量的想法,并表明应测试抗氧化补充剂作为改善肥胖妇女的IVF结果的手段。

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