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Racial Disparities in Metabolism, Central Obesity, and Sex Hormone-Binding Globulin in Postmenopausal Women¹

Division of Gerontology, Department of Medicine, University of Maryland School of Medicine, and Geriatric Research, Education, and Clinical Center, Baltimore Veterans Affair Medical Center, Baltimore, Maryland 21201

Address all correspondence and requests for reprints to: Dora M. Berman, Ph.D., Geriatric Research, Education, and Clinical Center (BT/18/GR), Baltimore Veterans Affairs Medical Center, 10 North Greene Street, Baltimore, Maryland 21201. E-mail: dberman{at}umaryland.edu

Increased total and intraabdominal fat (IAF) obesity as well as other metabolic conditions associated with the insulin resistance syndrome (IRS) are related to low levels of sex hormone-binding globulin (SHBG) in young and older Caucasian (CAU) and young African-American (AA) women. We examined whether postmenopausal AA women, a population with a high incidence of obesity and IRS despite low IAF, would have higher levels of circulating SHBG compared with CAU women, and whether there would be negative relationships between indexes of obesity and risk factors associated with IRS and SHBG levels. We measured body composition, SHBG, free testosterone, leptin, glucose tolerance, insulin, and lipoprotein lipids in 55 CAU (mean ± SD, 59 ± 7 yr) and 35 AA (57 ± 6 yr) sedentary women of comparable obesity (48% body fat, by dual energy x-ray absorptiometry). Compared with CAU women, AA women had larger waist (101 vs. 96 cm), larger fat mass (44.9 ± 8.8 vs. 39.9 ± 8.1 kg), larger sc fat area (552 ± 109 vs. 452 ± 109 cm²), and lower IAF/SC ratio (0.28 ± 0.12 vs. 0.38 ± 0.15; P < 0.01), but similar waist to hip ratio (0.83). Both groups had similar SHBG (117 vs. 124 nmol/L) and free testosterone (3.7 vs. 3.4 pmol/L) levels, but AA women had a 35% higher leptin, 34% higher fasting insulin, and 39% greater insulin response to a glucose load (P < 0.05) compared with CAU women. In CAU, but not AA, women SHBG correlated negatively with body mass index (r = -0.28; P < 0.05), waist (r = -0.36; P = 0.01), IAF (r = -0.34; P = 0.01), and insulin response to oral glucose (r = -0.37; P < 0.05) and positively with high density lipoprotein cholesterol (r = 0.30; P = 0.03). The relationship between insulin area and SHBG in CAU women disappeared after adjusting for IAF, whereas the relationship between high density lipoprotein cholesterol and SHBG persisted after adjusting for IAF, but not for fat mass. Leptin was positively related to fat mass (P < 0.05) in both groups, but it was related to insulin only in the Caucasian women (P < 0.01). There was a racial difference in the slopes (P < 0.05) of the relationships of leptin to fat mass (P < 0.05). Racial differences in leptin disappeared after adjustment for fasting insulin. These results suggest that the metabolic relationships between total and regional obesity, glucose, and lipid metabolism with SHBG in CAU women are different from those in postmenopausal obese AA women.

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