Associations of endogenous testosterone with cardiovascular risk factors

Several cross-sectional population studies found statistically significant correlations between plasma levels of testosterone and various risk factors, which, however, were opposite in men and women.

In men testosterone plasma levels were frequently found to have positive correlations with serum levels of HDL-C as well as inverse correlations with plasma levels of triglycerides, total cholesterol, LDL-C, fibrinogen and PAI-1. However, serum levels of testosterone have even stronger inverse correlations with BMI, waist circumference, waist-hip-ratio (WHR), amount of visceral fat and serum levels of leptin, insulin and free fatty acids. After adjustment for these measures of obesity and insulin resistance, the correlations between cardiovascular risk factors with testosterone but not with visceral fat or insulin lost their statistical significance (Hergenc et al. 1999; Tchernof et al. 1996; Tsai et al. 2000). These findings indicate that a low serum level of testosterone in eugonadal men is a component of the metabolic syndrome, which is characterized by the presence of obesity, glucose intolerance or overt type 2 diabetes mellitus, arterial hypertension, hypertriglyc-eridemia, low HDL-C, a pro-coagulatory and anti-fibrinolytic state and for which insulin resistance is thought to be an important etiological factor. Therefore, the frequently observed association of high testosterone levels with a more favourable cardiovascular risk factor profile in men probably does not reflect direct regulatory effects of testosterone on lipoprotein metabolism and the hemostatic system. Accordingly, in some populations these associations disappeared when serum levels of free testosterone (correcting for variations in SHBG) instead of total testosterone were correlated with lipids and other cardiovascular risk factors. Also in accordance with this, a low number of CAG repeats in the androgen receptor, which increases its sensitivity to testosterone, was associated with reduced levels of HDL-C and leptin as well as low body fat mass and body mass index (Zitzmann et al. 2001b; 2003). One reason for the discrepancy between the biological effects and the associations of endogenous testosterone with various cardiovascular risk factors is the negative regulatory effect of insulin on the production of sex hormone binding globulin so that insulin resistance causes low levels of sex hormone binding globulin and thereby low levels of total testosterone (Hautanen 2000).

Women present the opposite relationships between endogenous androgens and obesity, insulin and cardiovascular risk factors. In cross-sectional studies, serum levels of testosterone were found to have significant positive correlations with BMI and leptin levels. Low serum levels of SHBG, which is an indirect measure of female hyperandrogenism, were associated with high BMI and WHR as well as with high serum levels of leptin and insulin and low serum levels of HDL-C (Hergenc etal. 1999). Moreover, in a prospective study, 20% of women with SHBG-levels below the 5th percentile developed diabetes mellitus type 2 within the 12-year follow-up period (Lindstedt et al. 1991). Thus, in women, hyperandrogenism, rather than hypoandrogenism as in men, is a component of the insulin resistance syndrome. In agreement with this, women with PCOS frequently present with hypercholes-terolemia, low HDL-C, hypertriglyceridemia, elevated fibrinogen and PAI-1, and a family history of diabetes mellitus. Because many women with PCOS are overweight and most if not all are insulin resistant, it is a matter of debate whether these symptoms in women with PCOS are secondary to obesity and insulin resistance or whether hyperandrogenemia itself contributes to obesity, insulin resistance, and hyperinsulinemia (Amowitz and Sobel 1999; Dunaif 1997; Lobo and Carmina 2000; Rajkohowa etal. 2000).

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