4.7 Article

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

Journal

METABOLISM-CLINICAL AND EXPERIMENTAL
Volume 54, Issue 12, Pages 1626-1631

Publisher

W B SAUNDERS CO-ELSEVIER INC
DOI: 10.1016/j.metabol.2005.06.011

Keywords

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Funding

  1. NCRR NIH HHS [5M01RR00056, 2S07RR0541629] Funding Source: Medline
  2. NIDDK NIH HHS [DK-20411] Funding Source: Medline

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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 (homeostasis model assessment [HOMA] insulin sensitivity [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. (c) 2005 Elsevier Inc. All rights reserved.

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