RELATIONSHIP OF SEX-HORMONES TO LIPIDS AND LIPOPROTEINS IN NONDIABETIC MEN

RELATIONSHIP OF SEX-HORMONES TO LIPIDS AND LIPOPROTEINS IN NONDIABETIC MEN
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DOI:
10.1210/jc.77.6.1610
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发表时间:
1993-12-01
影响因子:
5.8
通讯作者:
KATZ, MS
KATZ, MS
中科院分区:
医学2区
文献类型:
--
作者:
HAFFNER, SM;MYKKANEN, L;KATZ, MS

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尽管许多研究表明,在绝经前和绝经后的女性中,雄激素原性的增加与甘油三酯(TG)的增加和高密度脂蛋白胆固醇的降低有关,但关于男性性激素与脂质和脂蛋白之间关系的数据相对较少。我们研究了来自圣安东尼奥心脏研究的178名非糖尿病男性的性激素结合球蛋白(SHBG)、总睾酮和游离睾酮、硫酸脱氢表雄酮(DHEA-SO4)和雌二醇与脂质和脂蛋白的关系,这是一项基于人群的糖尿病和心血管疾病研究。TG浓度与SHBG (r = -0.22)、游离睾酮(r = -0.15)、总睾酮(r = -0.22)、DHEA-SO4 (r = -0.16)呈显著负相关。高密度脂蛋白(HDL)胆固醇与SHBG (r = 0.21)、游离睾酮(r = 0.15)、总睾酮(I = 0.17)、DHEA-SO4 (r = 0.16)呈正相关。总睾酮与总胆固醇(r = -0.17)和低密度脂蛋白胆固醇(r = -0.15)显著相关。在调整年龄、体重指数、腰臀比、葡萄糖和胰岛素浓度后,TG浓度仍与SHBG (r = -0.20)、游离睾酮(r = -0.15)、DHEA-SO4 (r = -0.18)显著相关,HDL胆固醇仍与SHBG (r = 0.17)、游离睾酮(r = 0.15)、总睾酮(r = 0.14)、DHEA-SO4 (r = 0.16)显著相关。总之,我们观察到随着睾酮浓度的增加,致动脉粥样硬化的脂质和脂蛋白谱减少。这不能用葡萄糖或胰岛素浓度的差异来解释。然而,性激素只解释了总TG和高密度脂蛋白胆固醇浓度变化的一小部分。这些发现与女性的数据形成鲜明对比,在女性中,雄激素性的增加与TG的增加和高密度脂蛋白胆固醇水平的降低密切相关。
Although many studies show that increased androgenicity is associated with increased triglyceride (TG) and decreased high density lipoprotein cholesterol in both pre- and postmenopausal women, relatively few data are available on the association of sex hormones to lipids and lipoproteins in men. We examined the association of sex hormone-binding globulin (SHBG), total and free testosterone, dehydroepiandrosterone sulfate (DHEA-SO4), and estradiol with lipids and lipoproteins in 178 nondiabetic men from the San Antonio Heart Study, a population-based study of diabetes and cardiovascular disease. The TG concentration was significantly inversely related to SHBG (r = -0.22), free testosterone (r = -0.15), total testosterone (r = -0.22), and DHEA-SO4 (r = -0.16). High density lipoprotein (HDL) cholesterol was significantly positively correlated to SHBG (r = 0.21), free testosterone (r = 0.15), total testosterone (I = 0.17), and DHEA-SO4 (r = 0.16). Total testosterone was significantly related to total cholesterol (r = -0.17) and low density lipoprotein cholesterol (r = -0.15). After adjustment for age, body mass index, waist to hip ratio, and glucose and insulin concentrations, TG concentrations remained significantly related to SHBG (r = -0.20), free testosterone (r = -0.15), and DHEA-SO4 (r = -0.18), and HDL cholesterol remained significantly associated with SHBG (r = 0.17), free testosterone (r = 0.15), total testosterone (r = 0.14), and DHEA-SO4 (r = 0.16). In conclusion, we observed a less atherogenic lipid and lipoprotein profile with increased testosterone concentrations. This was not explained by differences in glucose or insulin concentrations. However, sex hormones explained only a small percentage of the variation in total TG and HDL cholesterol concentrations. These findings are in striking contrast to data from women, in whom increased androgenicity is strongly associated with increased TG and decreased HDL cholesterol levels.