Sidhwani Seema, Scoccia Bert, Sunghay Shwetha, Stephens-Archer Chantale N, Mazzone Theodore, Sam Susan
Department of Medicine, Section of Endocrinology, Diabetes and MetabolismDepartment of Obstetrics and GynecologyDepartment of Medicine, University of Illinois, Chicago, IL, USA.
Clin Endocrinol (Oxf). 2011 Jul;75(1):76-82. doi: 10.1111/j.1365-2265.2011.04015.x.
Adverse changes in lipoprotein particle number and size are common with insulin resistance and are associated with increased cardiovascular risk. Comprehensive information regarding lipoprotein particle number and size, and how these parameters relate to body weight, insulin resistance and hyperandrogenemia is lacking in polycystic ovary syndrome (PCOS). We tested the hypothesis that PCOS is associated with atherogenic changes in lipoprotein profile independent of body weight and examined the role of insulin resistance and androgens in these atherogenic changes.
Case-control study performed at Clinical Research Center at an Academic Medical Center in the United States.
Fasting blood was obtained from 25 PCOS and 25 control women of similar age and body mass index (BMI). Lipoprotein particle number and size was determined by nuclear magnetic resonance and compared between the groups.
The mean BMI for both groups was <30 kg/m(2) (P = 0·33). Women with PCOS had an increase in very low-density lipoprotein (VLDL) particle number (P = 0·005), low-density lipoprotein (LDL) particle number (P = 0·02) and a decrease in high-density lipoprotein (HDL) size (P = 0·04). LDL size was borderline decreased (P = 0·09). These differences persisted after adjustment for ethnicity, alcohol and tobacco intake and exercise. In stepwise regression models, bioavailable testosterone was the only predictor of LDL cholesterol, triglyceride, VLDL and LDL particle number. Sex hormone binding globulin (SHBG) was the only predictor of LDL and HDL size.
Independent of body weight, PCOS was associated with changes in lipoprotein profile that increases risk for cardiovascular disease. These changes were present in a mostly nonobese group of women and were more closely related to androgens than fasting insulin.
脂蛋白颗粒数量与大小的不良变化在胰岛素抵抗中很常见，且与心血管风险增加相关。多囊卵巢综合征（PCOS）患者缺乏关于脂蛋白颗粒数量与大小以及这些参数如何与体重、胰岛素抵抗和高雄激素血症相关的全面信息。我们检验了这样一个假设，即PCOS与脂蛋白谱的致动脉粥样硬化变化相关，且独立于体重，并研究了胰岛素抵抗和雄激素在这些致动脉粥样硬化变化中的作用。
在美国一家学术医疗中心的临床研究中心进行的病例对照研究。
从25名PCOS患者和25名年龄与体重指数（BMI）相似的对照女性中获取空腹血样。通过核磁共振测定脂蛋白颗粒数量与大小，并在两组之间进行比较。
两组的平均BMI均<30 kg/m²（P = 0·33）。PCOS女性的极低密度脂蛋白（VLDL）颗粒数量增加（P = 0·005）、低密度脂蛋白（LDL）颗粒数量增加（P = 0·02），高密度脂蛋白（HDL）大小减小（P = 0·04）。LDL大小临界减小（P = 0·09）。在对种族、酒精和烟草摄入量以及运动进行调整后，这些差异仍然存在。在逐步回归模型中，生物可利用睾酮是LDL胆固醇、甘油三酯、VLDL和LDL颗粒数量的唯一预测因子。性激素结合球蛋白（SHBG）是LDL和HDL大小的唯一预测因子。
独立于体重，PCOS与脂蛋白谱的变化相关，这些变化增加了心血管疾病风险。这些变化存在于大多数非肥胖女性群体中，并且与雄激素的关系比空腹胰岛素更为密切。
