School of Paediatrics and Reproductive Health, Robinson Institute, University of Adelaide, Adelaide, South Australia 5005, Australia.
J Reprod Immunol. 2011 Mar;88(2):142-8. doi: 10.1016/j.jri.2011.01.008. Epub 2011 Feb 17.
This review summarizes some of the recent advances in obesity research and describes how we and others have built upon these findings to better understand the impact of obesity on granulosa cells, cumulus cells and oocytes within the ovaries of obese females. Obesity is associated with lipid accumulation in non-adipose tissue cells and the induction of oxidative stress and endoplasmic reticulum stress responses that are tightly linked with systemic inflammation. Analysis of ovarian cells and fluid of obese women indicates that these same mechanisms are activated in the ovary in response to obesity. Studies in mice support this and allow further dissection of the pathways by which diet-induced obesity contributes to changes in mitochondria and the endoplasmic reticulum. These studies are in their infancy but cumulatively provide basic information about the cellular mechanisms that may lead to the impaired ovulation and reduced oocyte developmental potential that is observed in obese females.
本文综述了肥胖研究的一些最新进展，并描述了我们和其他人如何在此基础上进一步研究肥胖对肥胖女性卵巢中颗粒细胞、卵丘细胞和卵母细胞的影响。肥胖与非脂肪组织细胞中的脂质积累以及氧化应激和内质网应激反应的诱导有关，这些反应与全身炎症密切相关。对肥胖女性的卵巢细胞和液体的分析表明，这些相同的机制在卵巢中对肥胖做出反应而被激活。在小鼠中的研究支持这一点，并允许进一步剖析饮食诱导的肥胖如何导致线粒体和内质网变化的途径。这些研究还处于起步阶段，但它们累积提供了关于细胞机制的基本信息，这些机制可能导致肥胖女性中观察到的排卵障碍和卵母细胞发育潜能降低。
