Does androgen excess contribute to the cardiovascular risk profile in postmenopausal women with type 2 diabetes?

The purpose of this study was to determine if postmenopausal women with type 2 diabetes have clinical and biochemical evidence of androgen excess as a potential contributor to an increase in risk for coronary heart disease when compared with women without diabetes. Fasting glucose, insulin, lipids, sex hormone–binding globulin (SHBG), and sex steroids (from pooled samples) (total testosterone and free testosterone [non–SHBG-T], androstenedione [A-dione], total estrogens) were measured at baseline in 16 postmenopausal women with type 2 diabetes treated with diet or a sulfonylurea and 17 age-matched controls. Measurements of glucose, insulin, and sex steroids were repeated at hourly intervals for 3 hours after oral glucose administration. Hirsutism scores and insulin sensitivity (homeotasis model assessment [HOMA] insulin [SI]) were obtained. Women with type 2 diabetes were more hyperglycemic, hyperinsulinemic, and insulin-resistant (HOMA SI, 46.7 ± 7.0 vs 12.9 ± 2.0, P < .001), and had higher total to high-density lipoprotein cholesterol (TC/HDL) ratios, lower SHBG (20.8 ± 3.5 vs 59.3 ± 14.4 nmol/L, P < .05), higher non–SHBG-T (0.225 ± 0.025 vs 0.135 ± 0.021 nmol/L, P < .05), and higher hirsutism scores (1.1 ± 0.3 vs 0.3 ± 0.2, P = .004) than those without diabetes. No changes in sex steroids occurred after the oral glucose challenge. HOMA SI and area under the curve for glucose correlated significantly with SHBG ( r = −0.42), non–SHBG-T ( r = 0.40), and TC/HDL ( r = 0.41) (all P < .05) in the combined groups. Postmenopausal women with type 2 diabetes have both clinical and biochemical evidence of androgen excess that may contribute to more adverse cardiovascular risk profiles.