GEORGE SCHNEIDER,
MARVIN A. KIRSCHNER,
RICHARD BERKOWITZ and
NORMAN H. ERTEL
East Orange Veterans Administration Hospital, East Orange 07019; and the Newark Beth Israel Medical Center and the New Jersey Medical School, Newark, New Jersey 07112
Serum estrone (E,) and 17β-estradiol (E2) were noted tobe 2-fold elevated in a group of morbidly obese men. UrinaryE1 and E2 production rates were elevated in proportion to thedegree of obesity, with values as high as 127 and 157 µg/day,respectively.
Although serum testosterone (T) concentrations were reducedin obese men, averaging 348 ± 35 vs. 519 ± 42ng/dl in lean controls, the dialyzable T fractions were elevatedand, hence, the calculated free T concentrations were normalin obese men. Further, the obese men exhibited normal serumLH, FSH, and T responses to clomiphene citrate, indicating intacthypothalamic-pituitary-Leydig cell axes.
MCRs of T and peripheral conversion of T to E2 and androstenedione() to E1 were all increased in obese men in proportion to thepercentage above ideal weight.
Although the obese men exhibited increased blood levels andproduction rates of estrogens, there were no signs of feminization,increased T-estrogen-binding globulin levels, or suppressedbasal gonadotropin levels, suggesting a lack of biological effect.We postulate that obese men exhibit defective estrogen receptors,leading to decreased T-estrogen-binding globulin, increasedclearance of androgenic hormones, and elevated estrogen productionrates. (J Clin Endocrinol Metab48: 633, 1979)
* This work was presented in part at the 59th Meeting of The EndocrineSociety, Chicago, IL, 1977.
Received May 17, 1978.
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) to E1 were all increased in obese men in proportion to the percentage above ideal weight. 
