The Cholesterol, Metabolism, and Thrombosis Research Center, 3906 Middleton Avenue, Cincinnati, OH 45220, United States of America.
The Cholesterol, Metabolism, and Thrombosis Research Center, 3906 Middleton Avenue, Cincinnati, OH 45220, United States of America.
Metabolism. 2019 Mar;92:108-120. doi: 10.1016/j.metabol.2018.11.002. Epub 2018 Nov 13.
Polycystic ovary syndrome (PCOS) has multiple etiologies including ovarian and adrenal hyperandrogenism, neuro-endocrine and hypothalamic-pituitary dysfunction, and disorders of peripheral insulin resistance. Obesity is neither necessary nor sufficient for the PCOS phenotype, and the association of PCOS with obesity is not universal, with national, cultural, and ethnic differences. Obesity, particularly visceral adiposity which is common in obese and non-obese women with PCOS, amplifies and worsens all metabolic and reproductive outcomes in PCOS. Obesity increases insulin resistance and compensatory hyperinsulinemia, which in turn increases adipogenesis and decreases lipolysis. Obesity sensitizes thecal cells to LH stimulation and amplifies functional ovarian hyperandrogenism by upregulating ovarian androgen production. Obesity increases inflammatory adipokines which, in turn, increase insulin resistance and adipogenesis. Lifestyle interventions focused on diet-weight loss and concurrent exercise are central to therapy which also commonly subsequently needs to include pharmacologic therapy. PCOS symptoms commonly improve with 5% to 10% weight loss, but 25% to 50% weight loss, usually achievable only through bariatric surgery, may be required for morbid obesity unresponsive to lifestyle-medical treatment. Bariatric surgery is a valuable approach to weight loss in PCOS where BMI is ≥40 kg/m when non-surgical treatment and/or induction of pregnancy have failed, and can be an initial treatment when BMI is ≥50 kg/m. Further research in PCOS is needed to better understand the fundamental basis of the disorder, to ameliorate obesity, to correct hyperandrogenism, ovulation, hyperinsulinemia, and to optimize metabolic homeostasis.
多囊卵巢综合征（PCOS）有多种病因，包括卵巢和肾上腺雄激素过多症、神经内分泌和下丘脑-垂体功能障碍以及外周胰岛素抵抗紊乱。肥胖不是 PCOS 表型的必要条件，PCOS 与肥胖的相关性并不普遍，存在国家、文化和种族差异。肥胖，尤其是常见于肥胖和非肥胖的 PCOS 患者的内脏脂肪肥胖，放大和恶化了 PCOS 的所有代谢和生殖结局。肥胖会增加胰岛素抵抗和代偿性高胰岛素血症，进而增加脂肪生成并减少脂肪分解。肥胖使卵泡膜细胞对 LH 刺激敏感，并通过上调卵巢雄激素生成来放大功能性卵巢雄激素过多症。肥胖会增加炎症性脂肪因子，进而增加胰岛素抵抗和脂肪生成。以饮食-减重和同时运动为重点的生活方式干预是治疗的核心，通常随后还需要包括药物治疗。PCOS 症状通常会随着 5%至 10%的体重减轻而改善，但对于对生活方式-药物治疗无反应的病态肥胖，可能需要 25%至 50%的体重减轻，通常只有通过减肥手术才能实现。减肥手术是 PCOS 中一种有价值的减重方法，当 BMI≥40kg/m2 且非手术治疗和/或诱导妊娠失败时，或当 BMI≥50kg/m2 时，可以作为初始治疗方法。需要进一步研究 PCOS，以更好地了解该疾病的根本基础，改善肥胖症，纠正高雄激素血症、排卵、高胰岛素血症，并优化代谢稳态。
