Adipokinesand Ghrelin Rolein Regulation of Ovarian Function in Obesity

A. I. Abdusalamova, O. Bettikher, K. Rudenko, O. A. Belyaeva, A. Neimark, I. Zazerskaya
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Abstract

There is a great worldwide trend in the incidence of obesity, which is increasing with each passing year among all populations, including women of reproductive age. Given the impressive list of diseases associated with obesity, as well as the negative inverse correlation of the severity of obesity with fertility, this problem is global not only in the social sphere, but it also becomes demographically significant.Along with other pathogenetic mechanisms leading to persistent anovulation, an imbalance in adipokine production by adipose tissue can also serve as one of the important links in the development of reproductive dysfunction. Despite apparent interest in this topic, a large number of previously discovered adipokines are still not studied. Among adipokines, the effects of adiponectin and leptin on reproductive function are best known. Alterations in adiponectin and leptin levels can affect hypothalamic-pituitary-gonadal signaling, folliculogenesis, oogenesis and steroidogenesis. In addition, leptin is involved in the initiation of puberty, regulation of the menstrual cycle, and changes the balance between proliferation and apoptosis in ovarian cells. The leading causes of reduced fertility, infertility, and IVF failure in obese patients are mechanisms that promote the formation of chronic anovulation, delay the maturation of oocytes, reduce their quality, and/or lead to changes in endometrial susceptibility. These effects can be caused by an imbalance in the concentrations of leptin and adiponectin (leptin excess and adiponectin deficiency), lead to endometrial dysfunction, disruption of implantation and early embryogenesis. These changes, in turn, can affect just as the likelihood of spontaneous conception, so the effectiveness of assisted reproductive technologies and subsequent gestation.Thus, the study of potential pathogenetic pathways of fertility regulation in obesity, one of which is the subject of this review, is an important area for further study.
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肥胖患者卵巢功能的脂肪因子和胃饥饿素调节作用
肥胖的发病率在世界范围内有一个巨大的趋势,在所有人口中,包括育龄妇女,肥胖的发病率每年都在增加。鉴于与肥胖相关的疾病令人印象深刻的清单,以及肥胖的严重程度与生育率的负相关关系,这一问题不仅在社会领域是全球性的,而且在人口统计学上也具有重要意义。除了导致持续无排卵的其他病理机制外,脂肪组织产生脂肪因子的不平衡也可能是生殖功能障碍发展的重要环节之一。尽管人们对这个话题很感兴趣,但大量先前发现的脂肪因子仍未得到研究。在脂肪因子中,脂联素和瘦素对生殖功能的影响最为人所知。脂联素和瘦素水平的改变可影响下丘脑-垂体-性腺信号、卵泡生成、卵子生成和类固醇生成。此外,瘦素还参与青春期的开始,月经周期的调节,并改变卵巢细胞增殖和凋亡之间的平衡。肥胖患者生育能力下降、不孕和体外受精失败的主要原因是促进慢性无排卵形成、延迟卵母细胞成熟、降低卵母细胞质量和/或导致子宫内膜易感性改变的机制。这些影响可由瘦素和脂联素浓度失衡(瘦素过量和脂联素缺乏)引起,导致子宫内膜功能障碍,着床和早期胚胎发生中断。反过来,这些变化也会影响自然受孕的可能性,从而影响辅助生殖技术和后续妊娠的有效性。因此,研究肥胖中生育调节的潜在致病途径是一个重要的研究领域,也是本综述的主题之一。
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Obesity and Metabolism-Milan
Obesity and Metabolism-Milan 医学-内分泌学与代谢
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