Inflammation in Polycystic Ovary Syndrome: underpinning of insulin resistance and ovarian dysfunction.
Inflammation in Polycystic Ovary Syndrome: underpinning of insulin resistance and ovarian dysfunction.
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DOI：
10.1016/j.steroids.2011.12.003
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发表时间：
2012-03-10
期刊：
影响因子：
2.7
通讯作者：
González F
中科院分区：
文献类型：
--
作者：
González F
慢性低度炎症已成为多囊卵巢综合征（PCOS）发病机制的关键因素。饮食触发物如葡萄糖能够激发PCOS妇女单核细胞（MNC）的氧化应激和炎症反应，这种现象与肥胖无关。这是重要的，因为MNC衍生的巨噬细胞是过量脂肪组织中细胞因子产生的主要来源，并且还以旁分泌方式促进脂肪细胞细胞因子产生。促炎细胞因子肿瘤坏死因子-α（TNF α）是已知的胰岛素抵抗介质。多囊卵巢综合征患者糖刺激的MNC释放的TNF α沿着炎症分子标志物与胰岛素抵抗相关。高雄激素血症能够在空腹状态下激活MNC，从而增加MNC对葡萄糖的敏感性;这可能是促进PCOS饮食诱导的炎症的潜在机制。增加的腹部肥胖在PCOS的所有体重类别中普遍存在，并且这种发炎的脂肪组织有助于疾病中的炎症负荷。然而，葡萄糖摄入会引起正常体重PCOS女性的氧化应激，即使在没有增加腹部肥胖的情况下。在PCOS中，氧化应激和炎症标志物与循环雄激素高度相关。慢性抑制卵巢雄激素的产生并不能改善正常体重女性的炎症。此外，体外研究已经证明了促炎刺激物上调负责雄激素产生的卵巢卵泡膜细胞类固醇生成酶的能力。这些发现支持炎症直接刺激多囊卵巢产生雄激素的论点。
Chronic low-grade inflammation has emerged as a key contributor to the pathogenesis of Polycystic Ovary Syndrome (PCOS). A dietary trigger such as glucose is capable of inciting oxidative stress and an inflammatory response from mononuclear cells (MNC) of women with PCOS, and this phenomenon is independent of obesity. This is important because MNC-derived macrophages are the primary source of cytokine production in excess adipose tissue, and also promote adipocyte cytokine production in a paracrine fashion. The proinflammatory cytokine tumor necrosis factor-α (TNFα) is a known mediator of insulin resistance. Glucose-stimulated TNFα release from MNC along with molecular markers of inflammation are associated with insulin resistance in PCOS. Hyperandrogenism is capable of activating MNC in the fasting state, thereby increasing MNC sensitivity to glucose; and this may be a potential mechanism for promoting diet-induced inflammation in PCOS. Increased abdominal adiposity is prevalent across all weight classes in PCOS, and this inflamed adipose tissue contributes to the inflammatory load in the disorder. Nevertheless, glucose ingestion incites oxidative stress in normal weight women with PCOS even in the absence of increased abdominal adiposity. In PCOS, markers of oxidative stress and inflammation are highly correlated with circulating androgens. Chronic suppression of ovarian androgen production does not ameliorate inflammation in normal weight women with the disorder. Furthermore, in vitro studies have demonstrated the ability of pro-inflammatory stimuli to upregulate the ovarian theca cell steroidogenic enzyme responsible for androgen production. These findings support the contention that inflammation directly stimulates the polycystic ovary to produce androgens.
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