Dipartimento di Medicina e Chirurgia Traslazionale, Università Cattolica del Sacro Cuore, 00168 Rome, Italy.
Fondazione Policlinico Universitario a Gemelli IRCCS, 00168 Rome, Italy.
Int J Mol Sci. 2021 Feb 7;22(4):1667. doi: 10.3390/ijms22041667.
The pathophysiology of Polycystic Ovary Syndrome (PCOS) is quite complex and different mechanisms could contribute to hyperandrogenism and anovulation, which are the main features of the syndrome. Obesity and insulin-resistance are claimed as the principal factors contributing to the clinical presentation; in normal weight PCOS either, increased visceral adipose tissue has been described. However, their role is still debated, as debated are the biochemical markers linked to obesity per se. Oxidative stress (OS) and low-grade inflammation (LGI) have recently been a matter of researcher attention; they can influence each other in a reciprocal vicious cycle. In this review, we summarize the main mechanism of radical generation and the link with LGI. Furthermore, we discuss papers in favor or against the role of obesity as the first pathogenetic factor, and show how OS itself, on the contrary, can induce obesity and insulin resistance; in particular, the role of GH-IGF-1 axis is highlighted. Finally, the possible consequences on vitamin D synthesis and activation on the immune system are briefly discussed. This review intends to underline the key role of oxidative stress and low-grade inflammation in the physiopathology of PCOS, they can cause or worsen obesity, insulin-resistance, vitamin D deficiency, and immune dyscrasia, suggesting an inverse interaction to what is usually considered.
多囊卵巢综合征（PCOS）的病理生理学非常复杂，不同的机制可能导致高雄激素血症和排卵障碍，这是该综合征的主要特征。肥胖和胰岛素抵抗被认为是导致临床表现的主要因素；在正常体重的 PCOS 中，已经描述了内脏脂肪组织的增加。然而，它们的作用仍存在争议，正如与肥胖本身相关的生化标志物的作用仍存在争议一样。氧化应激（OS）和低度炎症（LGI）最近引起了研究人员的关注；它们可以在一个相互的恶性循环中相互影响。在这篇综述中，我们总结了自由基生成的主要机制及其与 LGI 的联系。此外，我们还讨论了支持或反对肥胖作为最初发病因素的作用的论文，并展示了 OS 本身如何反过来引起肥胖和胰岛素抵抗；特别强调了 GH-IGF-1 轴的作用。最后，简要讨论了维生素 D 合成和激活对免疫系统的可能影响。这篇综述旨在强调氧化应激和低度炎症在 PCOS 病理生理学中的关键作用，它们可以导致或加重肥胖、胰岛素抵抗、维生素 D 缺乏和免疫功能紊乱，表明与通常认为的相反存在相互作用。
