Kalish Grace Mariko, Barrett-Connor Elizabeth, Laughlin Gail A, Gulanski Barbara I
Yale University School of Medicine, New Haven, Connecticut 06510-8046, USA.
J Clin Endocrinol Metab. 2003 Apr;88(4):1646-52. doi: 10.1210/jc.2002-021375.
Most studies of sex hormones and insulin resistance (IR) have focused on androgens; few have examined the association of endogenous estrogens and IR. We determined the cross-sectional association of endogenous levels of total and bioavailable testosterone and estradiol and SHBG with IR among 845 healthy, postmenopausal women aged 45-65 yr. Women were within 10 yr of menopause and not using hormone replacement therapy. Total adiposity was estimated by body mass index, visceral adiposity by waist to hip ratio (WHR), and IR by the homeostasis model assessment. We defined homeostasis model assessment-IR as the highest quartile (cutpoint, 2.1) of the distribution in this cohort. In logistic regression analyses, the odds for IR were significant and increased in a dose-response fashion across each quartile of total estradiol, bioavailable estradiol, and bioavailable testosterone (all P < 0.001 for linear trend). These associations remained significant after adjusting for WHR; adjusted odds ratios were 4.0, 6.1, and 2.7 for total estradiol, bioavailable estradiol, and bioavailable testosterone, respectively, comparing the highest to the lowest quartile (all P < 0.001). Adjusting for body mass index and WHR together eliminated the linear association of IR with total estradiol and bioavailable testosterone, but the association with bioavailable estradiol remained (adjusted odds ratio, 2.7; P < 0.001, comparing the highest to the lowest quartile). IR was not associated with total testosterone before or after adjusting for adiposity. Lower SHBG levels were associated with higher odds of IR, independent of adiposity. These results suggest that estrogen may be equally or more important than testosterone in the pathway to IR in healthy, young postmenopausal women, with differences not entirely explained by body size.
大多数关于性激素与胰岛素抵抗（IR）的研究都集中在雄激素上；很少有研究探讨内源性雌激素与IR之间的关联。我们确定了845名年龄在45 - 65岁的健康绝经后女性中，总睾酮、生物可利用睾酮、雌二醇的内源性水平以及性激素结合球蛋白（SHBG）与IR之间的横断面关联。这些女性处于绝经后10年内，且未使用激素替代疗法。通过体重指数估算总体脂，通过腰臀比（WHR）估算内脏脂肪，通过稳态模型评估法评估IR。我们将稳态模型评估-IR定义为该队列分布中最高四分位数（切点为2.1）。在逻辑回归分析中，IR的比值比具有显著性，并且随着总雌二醇、生物可利用雌二醇和生物可利用睾酮的每个四分位数呈剂量反应方式增加（线性趋势的所有P < 0.001）。在调整WHR后，这些关联仍然显著；将最高四分位数与最低四分位数相比，总雌二醇、生物可利用雌二醇和生物可利用睾酮的调整后比值比分别为4.0、6.1和2.7（所有P < 0.001）。同时调整体重指数和WHR消除了IR与总雌二醇和生物可利用睾酮的线性关联，但与生物可利用雌二醇的关联仍然存在（调整后比值比为2.7；将最高四分位数与最低四分位数相比，P < 0.001）。在调整肥胖因素之前或之后，IR与总睾酮均无关联。较低的SHBG水平与IR的较高比值比相关，且独立于肥胖因素。这些结果表明，在健康的年轻绝经后女性通往IR的途径中，雌激素可能与睾酮同样重要或更为重要，且差异并不完全由体型来解释。
