多囊卵巢综合征与肥胖:一种现代范式

M. Khamoshina, Yu.S. Artemenko, Ayshan A. Bayramova, Valentina A. Ryabova, M. Orazov
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引用次数: 0

摘要

多囊卵巢综合征是一种影响育龄妇女的异质性内分泌疾病。到目前为止,多囊卵巢综合征的发病机制尚未得到充分研究,其范式考虑了激素和代谢紊乱表现的遗传决定论,这被认为是超声检查(超声)期间验证该疾病(高雄激素血症、少排卵/无排卵和/或多囊卵巢转化)的标准。这篇综述讨论了高雄激素血症、胰岛素抵抗和肥胖之间相互作用的主要途径及其在多囊卵巢综合征发病机制中的作用,以及这类患者的可能治疗方法。这篇综述分析了高雄激素血症和胰岛素抵抗在实施多囊卵巢综合征遗传方案中的作用,并找出了患有多囊卵巢综合症的女性经常表现出“代谢三重”——高胰岛素血症、胰岛素抵抗和2型糖尿病的原因。值得注意的是,肥胖不包括在多囊卵巢综合征的诊断标准中,但流行病学数据证实了这些疾病之间存在关系。肥胖,尤其是内脏肥胖,通常发生在多囊卵巢综合征女性身上,会增强和恶化多囊卵巢综合症的代谢和生殖结果,并增加胰岛素抵抗和代偿性高胰岛素血症,进而刺激脂肪生成并抑制脂解。肥胖增加了科技细胞对黄体生成素刺激的敏感性,并增强了卵巢的功能性高雄激素血症,增加了卵巢雄性激素的产生。超重与大量炎症性脂肪因子有关,这些因子反过来又会导致胰岛素抵抗和脂肪生成。肥胖和胰岛素抵抗会加剧高雄激素血症的症状,形成恶性循环,导致多囊卵巢综合征的发展。这些数据使我们能够得出结论,减肥手术可以成为药物(二甲双胍、胰高血糖素样肽-1的噻唑烷二酮类似物)的替代品,该药物在治疗多囊卵巢综合征和肥胖患者方面显示出积极效果。
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Polycystic ovary syndrome and obesity: a modern paradigm
Polycystic ovary syndrome is a heterogeneous endocrine disease that affects women of childbearing age. The pathogenesis of polycystic ovary syndrome has not been fully studied to date, its paradigm considers the genetic determinism of the manifestation of hormonal and metabolic disorders, which are considered to be criteria for the verification of the disease (hyperandrogenism, oligo/anovulation and/or polycystic ovarian transformation during ultrasound examination (ultrasound). This review discusses the main ways of interaction between hyperandrogenism, insulin resistance and obesity and their role in the pathogenesis of polycystic ovary syndrome, as well as possible methods of treatment for this category of patients. The review analyzes the role of hyperandrogenism and insulin resistance in the implementation of the genetic scenario of polycystic ovary syndrome and finds out the reasons why women with polycystic ovary syndrome often demonstrate the presence of a «metabolic trio» - hyperinsulinemia, insulin resistance and type 2 diabetes mellitus. It is noted that obesity is not included in the criteria for the diagnosis of polycystic ovary syndrome, but epidemiological data confirm the existence of a relationship between these diseases. Obesity, especially visceral, which is often found in women with polycystic ovary syndrome, enhances and worsens metabolic and reproductive outcomes with polycystic ovary syndrome, as well as increases insulin resistance and compensatory hyperinsulinemia, which, in turn, stimulates adipogenesis and suppresses lipolysis. Obesity increases the sensitivity of tech cells to luteinizing hormone stimulation and enhances functional hyperandrogenism of the ovaries, increasing the production of androgens by the ovaries. Excess body weight is associated with a large number of inflammatory adipokines, which, in turn, contribute to the growth of insulin resistance and adipogenesis. Obesity and insulin resistance exacerbate the symptoms of hyperandrogenism, forming a vicious circle that contributes to the development of polycystic ovary syndrome. These data allow us to conclude that bariatric surgery can become an alternative to drugs (metformin, thiazolidinedione analogs of glucagon-like peptide-1), which has shown positive results in the treatment of patients with polycystic ovary syndrome and obesity.
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0.50
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发文量
43
审稿时长
8 weeks
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