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Glucose and lipopolysaccharide regulate proatherogenic cytokine release from mononuclear cells in polycystic ovary syndrome

机译：葡萄糖和脂多糖调节多囊卵巢综合征中单核细胞的促动脉粥样硬化细胞因子释放

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Women with polycystic ovary syndrome (PCOS) have chronic low-grade inflammation, which can increase the risk of atherogenesis. We examined the effect of glucose ingestion and lipopolysaccharide (LPS) on markers of proatherogenic inflammation in the mononuclear cells (MNC) and plasma of women with PCOS. Sixteen women with PCOS (8 lean, 8 obese) and 15 weight-matched controls (8 lean, 7 obese) underwent a 3-h oral glucose tolerance test (OGTT). Interleukin-6 (IL-6) and interleukin-1β (IL-1β) release from MNC cultured in the presence of LPS and plasma IL-6, C-reactive protein (CRP), and soluble vascular adhesion molecule-1 (sVCAM-1) were measured from blood samples drawn while fasting and 2 h after glucose ingestion. Truncal fat was measured by dual-energy absorptiometry (DEXA). Lean women with PCOS and obese controls failed to suppress LPS-stimulated IL-6 and IL-1β release from MNC after glucose ingestion. In contrast, obese women with PCOS suppressed these MNC-derived cytokines under the same conditions. In response to glucose ingestion, plasma IL-6 and sVCAM-1 increased and CRP suppression was attenuated in both PCOS groups and obese controls compared with lean controls. Fasting plasma IL-6 and CRP correlated positively with percentage of truncal fat. The absolute change in plasma IL-6 correlated positively with testosterone. We conclude that glucose ingestion promotes proatherogenic inflammation in PCOS with a systemic response that is independent of obesity. Based on the suppressed MNC-derived cytokine responses suggestive of LPS tolerance, chronic low-grade inflammation may be more profound in obese women with PCOS. Excess abdominal adiposity and hyperandrogenism may contribute to atherogenesis in PCOS.
机译：多囊卵巢综合征（PCOS）的女性患有慢性低度炎症，这会增加动脉粥样硬化的风险。我们检查了葡萄糖摄入和脂多糖（LPS）对PCOS妇女单核细胞（MNC）和血浆中促动脉粥样硬化炎症标志物的影响。十六名患有PCOS的妇女（8例瘦身，8肥胖）和15名体重匹配的对照组（8例瘦身，7肥胖）进行了3小时的口服葡萄糖耐量测试（OGTT）。白细胞介素6（IL-6）和白细胞介素1β（IL-1β）从LPS和血浆中的IL-6，C反应蛋白（CRP）和可溶性血管黏附分子1（sVCAM- 1）是在禁食和摄取葡萄糖2小时后从抽取的血液样本中测量的。腹部脂肪通过双能吸收法（DEXA）测量。患有PCOS和肥胖控制的瘦妇女在葡萄糖摄入后未能抑制LPS刺激的MNC释放IL-6和IL-1β。相比之下，患有PCOS的肥胖女性在相同条件下抑制了这些MNC衍生的细胞因子。响应葡萄糖摄入，与瘦对照组相比，PCOS组和肥胖对照组的血浆IL-6和sVCAM-1增加，CRP抑制作用减弱。空腹血浆IL-6和CRP与截短脂肪百分比呈正相关。血浆IL-6的绝对变化与睾丸激素呈正相关。我们得出的结论是，葡萄糖摄入可促进PCOS的促动脉粥样硬化炎症，其全身反应与肥胖无关。基于暗示对LPS耐受的MNC衍生的细胞因子抑制作用，肥胖的PCOS女性的慢性低度炎症可能更为严重。过多的腹部肥胖和雄激素过多可能会导致PCOS的动脉粥样硬化。

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