Serum estrone (E1) and 17beta-estradiol (E2) were noted to be 2-fold elevated in a group of morbidly obese men. Urinary E1 and E2 production rates were elevated in proportion to the degree of obesity, with values as high as 127 and 157 micrograms/day, respectively. Although serum testosterone (T) concentrations were reduced in obese men, averaging 348 +/- 35 vs. 519 +/- 42 ng/dl in lean controls, the dialyzable T fractions were elevated and, hence, the calculated free T concentrations were normal in obese men. Further, the obese men exhibited normal serum LH, FSH, and T responses to clomiphene citrate, indicating intact hypothalamic-pituitary-Leydig cell axes. MCRs of T and peripheral conversion of T to E2 and androstenedione (delta) to E1 were all increased in obese men in proportion to the percentage above ideal weight. Although the obese mean exhibited increased blood levels and production rates of estrogens, there were no signs of feminization, increased T-estrogen-binding, globulin levels, or suppressed basal gonadotropin levels, suggesting a lack of biological effect. We postulate that obese men exhibit defective estrogen receptors, leading to decreased T-estrogen-binding globulin, increased clearance of androgenic hormones, and elevated estrogen production rates.

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Androgen and estrogen production rates were examined in 29 morbidly obese women with upper or lower body obesity. Although blood production rates of testosterone (T), dihydrotestosterone, and androstenedione (A4) were elevated in all of these women, those with upper body obesity (waist-height ratios, greater than 0.85) had higher T and production rates than women with lower body obesity (waist-height ratio less than 0.75). A4 was equally elevated in women with upper and lower body obesity. Peripheral aromatization of A4 to estrone (E1) averaged 1.67% in women with upper body obesity, but was elevated at 2.54% in women with lower body obesity. Urinary E1 production rates averaged 466 +/- 295 nmol/day (172 +/- 109 micrograms/day) in women with upper body obesity. Thus, women with lower body obesity had higher E1 production rates due entirely to increased peripheral aromatization. Women with upper body obesity were observed to have higher serum T and estradiol (E2) levels than women with lower body obesity. Further, upper body obesity was associated with decreased levels of sex hormone-binding globulin (16.1 +/- 5.7 nmol/L vs. 18.9 +/- 6.1 in women with lower body obesity). As a result, free T levels averaged 98.8 +/- 39.2 pmol/L in women with upper body obesity vs. 82.2 +/- 33 in women with lower body obesity. Similarly, serum free E2 levels were higher in women with upper body vs. lower body obesity. The data demonstrate that sex hormone production and metabolism are different in morbidly obese women with these differing phenotypes. Women with upper body obesity have higher androgen production rates and higher free T and free E2 levels, whereas women with lower body obesity make increased amounts of E1 from peripheral aromatization. The biological significance of increased aromatization may be offset by increased free E2 levels in women with upper body obesity.