Parental diet-induced obesity leads to retarded early mouse embryo development and altered carbohydrate utilisation by the blastocyst
Parental diet-induced obesity leads to retarded early mouse embryo development and altered carbohydrate utilisation by the blastocyst
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DOI：
10.1071/rd11256
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发表时间：
2012-01-01
影响因子：
1.9
通讯作者：
Gardner, David K.
中科院分区：
文献类型：
--
作者：
Binder, Natalie K.;Mitchell, Megan;Gardner, David K.
母亲肥胖会导致生殖并发症，而父亲肥胖的影响尚不清楚。本研究探讨了双亲肥胖对着床前胚胎细胞周期长度和碳水化合物利用的影响。通过从正常或肥胖的C57BL/6雌性小鼠与正常的瑞士雄性小鼠(母亲肥胖)交配，或从正常的瑞士雌性小鼠与正常或肥胖的C57BL/6雄性小鼠交配(父亲肥胖)获得受精卵，独立地评估母亲和父亲的肥胖。受精卵在体外培养，然后用时间推移显微镜评估发育情况，并用超微荧光测定代谢。母体肥胖与压实前细胞周期动力学从1-细胞阶段显著延迟有关。虽然糖酵解保持不变，但与正常女性相比，肥胖女性胚胎的葡萄糖消耗量在压缩后显著增加。同样，父亲的肥胖导致植入前胚胎发育过程中细胞周期进程的显著延迟。然而，这种发育延迟是从胚胎基因组激活后的第二卵裂阶段开始观察到的。来自肥胖男性的胚泡表现出不成比例的碳水化合物代谢变化，糖酵解显著增加。总体而言，代谢变化对胚泡的形成没有抑制作用；然而，当父母中的任何一方肥胖时，胚泡细胞数量显著减少。这些数据表明，母亲和父亲的肥胖都显著影响着植入前的胚胎生理。
Maternal obesity results in reproductive complications, whereas the impact of paternal obesity is unclear. In the present study, the effects of parental obesity on preimplantation embryo cell cycle length and carbohydrate utilisation were investigated. Maternal and paternal obesity were assessed independently by deriving zygotes from normal or obese C57BL/6 female mice mated with normal Swiss male mice (maternal obesity), or from normal Swiss female mice mated with normal or obese C57BL/6 male mice (paternal obesity). Zygotes were cultured in vitro and development was then assessed by time-lapse microscopy and metabolism determined using ultramicrofluorescence. Maternal obesity was associated with a significant delay in precompaction cell cycle kinetics from the 1-cell stage. A significant increase in glucose consumption by embryos from obese compared with normal females occurred after compaction, although glycolysis remained unchanged. Similarly, paternal obesity led to significant delays in cell cycle progression during preimplantation embryo development. However, this developmental delay was observed from the second cleavage stage onwards, following embryonic genome activation. Blastocysts from obese males showed disproportionate changes in carbohydrate metabolism, with significantly increased glycolysis. Overall, metabolic changes were not inhibitory to blastocyst formation; however, blastocyst cell numbers were significantly lower when either parent was obese. These data suggest that both maternal and paternal obesity significantly impacts preimplantation embryo physiology.