Background

Polycystic ovary syndrome (PCOS) is the most common endocrinopathy among reproductive age women. Although its cardinal manifestations include hyperandrogenism, oligo/anovulation, and/or polycystic ovarian morphology, PCOS women often display also notable metabolic comorbidities. An array of pathogenic mechanisms have been implicated in the etiology of this heterogeneous endocrine disorder; hyperandrogenism at various developmental periods is proposed as a major driver of the metabolic and reproductive perturbations associated with PCOS. However, the current understanding of the pathophysiology of PCOS-associated metabolic disease is incomplete, and therapeutic strategies used to manage this syndrome's metabolic complications remain limited.

Scope of review

This study is a systematic review of the potential etiopathogenic mechanisms of metabolic dysfunction frequently associated with PCOS, with special emphasis on the metabolic impact of androgen excess on different metabolic tissues and the brain. We also briefly summarize the therapeutic approaches currently available to manage metabolic perturbations linked to PCOS, highlighting current weaknesses and future directions.

Major conclusions

Androgen excess plays a prominent role in the development of metabolic disturbances associated with PCOS, with a discernible impact on key peripheral metabolic tissues, including the adipose, liver, pancreas, and muscle, and very prominently the brain, contributing to the constellation of metabolic complications of PCOS, from obesity to insulin resistance. However, the current understanding of the pathogenic roles of hyperandrogenism in metabolic dysfunction of PCOS and the underlying mechanisms remain largely incomplete. In addition, the development of more efficient, even personalized therapeutic strategies for the metabolic management of PCOS patients persists as an unmet need that will certainly benefit from a better comprehension of the molecular basis of this heterogeneous syndrome.

中文翻译：

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多囊卵巢综合征的代谢功能障碍：雄激素过多的致病作用和潜在的治疗策略。

背景

多囊卵巢综合征（PCOS）是育龄妇女中最常见的内分泌病。尽管其主要表现包括雄激素过多，无排卵和/或多囊卵巢形态，但PCOS妇女通常还表现出明显的代谢合并症。多种致病机制与这种异质内分泌疾病的病因有关。提出了处于不同发育时期的雄激素过多症是与PCOS相关的代谢和生殖摄动的主要驱动力。但是，目前对与PCOS相关的代谢性疾病的病理生理学的了解还不完整，用于治疗该综合征的代谢性并发症的治疗策略仍然有限。

审查范围

这项研究是对与PCOS经常相关的代谢功能异常的潜在病因机制的系统综述，特别着重于雄激素过量对不同代谢组织和大脑的代谢影响。我们还简要概述了目前可用于管理与PCOS相关的代谢紊乱的治疗方法，突出了当前的弱点和未来的方向。

主要结论

雄激素过多在与PCOS相关的代谢紊乱的发展中起着重要作用，对关键的周围代谢组织（包括脂肪，肝，胰腺和肌肉，尤其是大脑）有明显的影响，有助于代谢并发症的发生。从肥胖到胰岛素抵抗。但是，目前对高雄激素血症在PCOS代谢功能障碍中的致病作用及其潜在机制的了解仍然不完整。另外，仍存在针对PCOS患者代谢管理的更有效，甚至个性化治疗策略的发展，这是一项尚未得到满足的需求，当然，这将得益于对这种异质综合征的分子基础的更好理解。