Sarfati J, Young J, Christin-Maitre S
Service d'Endocrinologie et des Maladies de la Reproduction, Centre Hospitalier Universitaire de Bicêtre - APHP, 78 rue du Général-Leclerc 94275 Le Kremlin-Bicêtre, France.
Ann Endocrinol (Paris). 2010 Sep;71 Suppl 1:S49-53. doi: 10.1016/S0003-4266(10)70007-X.
Weight, fat mass and obesity have been shown to play a major role in female reproduction. Obese women have a greater risk than nonobese women of infertility and they fail to become pregnant in both natural and assisted conception cycles. This cannot be explained only by their lack of ovulation. There are several potential mechanisms. On one hand, the endometrium seems to be partially responsible for this low fecundity in obese women. On the other hand, the oocyte seems to be implied. In a model of obese mouse, maternal obesity prior to conception is associated with altered mitochondria in mouse oocytes and an increased generation of reactive oxygen species (ROS). Furthermore, compared with controls, obese mice have significantly more decreased embryonic IGF-IR staining, smaller fetuses and smaller pups. In this model, all weaned pups have been fed with a regular diet. At 13 weeks, pups delivered from obese mice were significantly larger, and these pups demonstrated early development of a metabolic-type syndrome. These findings suggest that maternal obesity has adverse effects as early as the oocyte and preimplantation embryo stages and that these effects may contribute to lasting morbidity in offspring, underscoring the importance of optimal maternal weight and nutrition before conception.
体重、脂肪量和肥胖已被证明在女性生殖中起主要作用。肥胖女性比非肥胖女性不孕的风险更高，并且在自然受孕和辅助受孕周期中都难以怀孕。这不能仅用她们不排卵来解释。有几种潜在机制。一方面，子宫内膜似乎是肥胖女性生育力低下的部分原因。另一方面，卵母细胞似乎也有影响。在肥胖小鼠模型中，受孕前母体肥胖与小鼠卵母细胞线粒体改变以及活性氧（ROS）生成增加有关。此外，与对照组相比，肥胖小鼠的胚胎胰岛素样生长因子1受体（IGF-IR）染色显著减少，胎儿和幼崽更小。在这个模型中，所有断奶幼崽都喂食常规饮食。13周时，肥胖小鼠所生的幼崽明显更大，并且这些幼崽表现出代谢型综合征的早期发展。这些发现表明，母体肥胖早在卵母细胞和植入前胚胎阶段就有不良影响，并且这些影响可能导致后代持续发病，强调了受孕前母体最佳体重和营养的重要性。
