Hyperinsulinemia and sex hormones in healthy premenopausal women: Relative contribution of obesity, obesity type, and duration of obesity

Hyperinsulinemia and sex hormones in healthy premenopausal women: Relative contribution of obesity, obesity type, and duration of obesity
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DOI:
10.1016/s0026-0495(98)90186-x
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发表时间:
1998-01-01
影响因子:
9.8
通讯作者:
Juric, M
Juric, M
中科院分区:
医学1区
文献类型:
--
作者:
Ivandic, A;Prpic-Krizevac, I;Juric, M

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胰岛素分泌对口服葡萄糖耐量试验(OGTT)和性激素水平的反应在49名健康肥胖绝经前妇女中评估了游离睾酮、雄烯二酮、硫酸脱氢表雄酮[DHEAS]、雌二醇和性激素结合球蛋白[SHBG(体重指数[BMI],30至50.6 kg/m2)和21名对照组受试者(BMI,17.8至24.0 kg/m2),葡萄糖耐量正常,无高雄激素血症体征。根据腰臀比(WHR)将肥胖妇女分为上半身肥胖组(WHR > 0.85)27例和下半身肥胖组(WHR <0.8)22例。上半身肥胖组空腹胰岛素和葡萄糖诱导胰岛素水平均高于对照组(P <0.001)和下半身肥胖组(P <0.001)。在上半身肥胖的女性中观察到高雄激素血症,这通过显著升高的游离睾酮(P <0.05 v对照组和下半身肥胖的受试者)和降低的SHBG(P <0.001 v对照组)来证明。空腹胰岛素水平最重要的独立决定因素是BMI(P <0.01)和DHEAS与游离睾酮的比值(P <0.01)。累积胰岛素反应最重要的决定因素是腰臀比(P <0.0005)、肥胖持续时间(P <0.01)和雄烯二酮水平(P <0.01)。总之,在没有高雄激素血症临床体征的健康肥胖绝经前妇女中,高BMI和更明显的上身脂肪定位导致高胰岛素血症和高雄激素血症。肥胖的持续时间夸大了葡萄糖诱导的胰岛素水平和累积胰岛素反应,而与肥胖程度和肥胖类型无关。DHEAS与游离睾酮的比值是空腹胰岛素浓度的独立决定因素。此外,DHEAS与游离睾酮的比例,而不是单独的这些雄激素中的任何一种,可能在调节女性胰岛素作用中很重要。版权所有(C)1998由W.B.桑德斯公司
Insulin secretion in response to an oral glucose tolerance test (OGTT) and sex hormone levels (free testosterone, androstenedione, dehydroepiandrosterone sulfate [DHEAS], estradiol, and sex hormone-binding globulin [SHBG]) were evaluated in 49 healthy obese premenopausal women (body mass index [BMI], 30 to 50.6 kg/m(2)) and 21 control subjects (BMI, 17.8 to 24.0 kg/m(2)) with normal glucose tolerance and without signs of hyperandrogenism. Obese women were divided into two groups according to waist to hip ratio (WHR): 27 subjects with upper-body obesity (WHR > 0.85) and 22 subjects with lower-body obesity (WHR < 0,8), Both fasting and glucose-induced insulin levels were higher in women with upper-body obesity than in controls (P < .001) and those with lower-body obesity (P < .001). Hyperandrogenism was observed in women with upper-body obesity, as evident by significantly elevated free testosterone (P < .05 v controls and subjects with lower-body obesity) and decreased SHBG (P < .001 v controls). The most important independent determinants of fasting insulin levels were BMI (P < .01) and the ratio of DHEAS to free testosterone (P < .01). The most important determinants of cumulative insulin response were WHR (P < .0005), duration of obesity (P < .01), and androstenedione levels (P < .01). In conclusion, in healthy obese premenopausal women without clinical signs of hyperandrogenism, a high BMI and more pronounced upper-body fat localization resulted in hyperinsulinemia and hyperandrogenism. The duration of obesity exaggerated the glucose-induced insulin level and cumulative insulin response independently of the degree of obesity and obesity type. The ratio of DHEAS to free testosterone was an independent determinant of fasting insulin concentration. Furthermore, the ratio of DHEAS to free testosterone rather than either of these androgens alone may be important in the regulation of insulin action in women. Copyright (C) 1998 by W.B. Saunders Company.