Haffner S M
Department of Medicine, University of Texas Health Science Center at San Antonio 78284-7873 USA.
Horm Res. 1996;45(3-5):233-7. doi: 10.1159/000184794.
Possible data complicating sex hormones, especially testosterone, in the etiology of cardiovascular disease and noninsulin-dependent diabetes mellitus (NIDDM) comes from the much higher rates of cardiovascular disease in men than in women. Pharmacological administration of anabolic steroids to both men and women increases glucose and insulin concentrations and also insulin resistance. In vivo assessment of sex hormones and binding proteins in both premenopausal and postmenopausal women has suggested that increased free testosterone and decreased sex hormone-binding globulin (SHBG) is associated with higher glucose and insulin concentrations. In a few studies, increased insulin resistance has been associated with decreased SHBG levels. Some data suggests that visceral fat mediated the associates of sex hormones with insulin in women. Little prospective data is available on the association of sex hormones to the development of NIDDM in women but in two studies, low SHBG concentrations predicted NIDDM in Gothenburg and San Antonio. Recently, attention has focused on the role of sex hormones in relation to insulin in men. Surprisingly, higher levels of testosterone have been associated with improved cardiovascular risk factors (such as high-density lipoprotein cholesterol) and lower glucose and insulin levels. Total testosterone and SHBG have been associated with defects in nonoxidative glucose disposal and upper body adiposity in normoglycemic Finnish men. The latter observation is of interest since specific defects in nonoxidative glucose disposal are observed in normoglycemic relatives of subjects with NIDDM. The temporal relationship between sex hormones and insulin has been controversial. The traditional view of sex hormones increasing insulin resistance has been challenged in women by studies showing that insulin stimulates androgen production in the ovary. Recent data [JCEM 1995;80:654-658] suggests that insulin stimulates testosterone production and suppresses SHBG production in normal and obese men. On the other hand, administration of testosterone to centrally obese hypogonadal middle-aged men has improved insulin sensitivity.
在心血管疾病和非胰岛素依赖型糖尿病（NIDDM）病因中，可能使性激素尤其是睾酮情况复杂化的数据源于男性心血管疾病发病率远高于女性。对男性和女性进行合成代谢类固醇的药物给药会增加葡萄糖和胰岛素浓度，同时也会增加胰岛素抵抗。对绝经前和绝经后女性体内性激素及结合蛋白的评估表明，游离睾酮增加和性激素结合球蛋白（SHBG）降低与更高的葡萄糖和胰岛素浓度相关。在一些研究中，胰岛素抵抗增加与SHBG水平降低有关。一些数据表明，内脏脂肪介导了女性性激素与胰岛素之间的关联。关于女性性激素与NIDDM发生之间的关联，几乎没有前瞻性数据，但在两项研究中，低SHBG浓度可预测哥德堡和圣安东尼奥的NIDDM。最近，人们关注到了性激素在男性体内与胰岛素的关系。令人惊讶的是，较高水平的睾酮与改善心血管危险因素（如高密度脂蛋白胆固醇）以及较低的葡萄糖和胰岛素水平相关。总睾酮和SHBG与血糖正常的芬兰男性非氧化葡萄糖处理缺陷及上身肥胖有关。后一观察结果很有意思，因为在NIDDM患者的血糖正常亲属中也观察到了非氧化葡萄糖处理的特定缺陷。性激素与胰岛素之间的时间关系一直存在争议。传统观点认为性激素会增加胰岛素抵抗，但在女性中，一些研究对这一观点提出了挑战，这些研究表明胰岛素会刺激卵巢产生雄激素。最近的数据[《临床内分泌与代谢杂志》1995年；80：654 - 658]表明，胰岛素会刺激正常和肥胖男性的睾酮生成并抑制SHBG生成。另一方面，对中心性肥胖的性腺功能减退中年男性给予睾酮可改善胰岛素敏感性。
