Excess body fat has been clearly associated with an increased risk of oligo-ovulation and endometrial/breast carcinoma. The connection has been assumed to lie within derangements of the metabolic/endocrine compartments, particularly of of estrogens and androgens. To differentiate the effect obesity from its related disease process, an attempt has been made to define the reproductive-endocrinologic alterations encountered in otherwise asymptomatic obese women. Androgen metabolism is accelerated in obesity. It is not clear whether the increased clearance precedes or follows the accelerated production of androgens. A servocontrol mechanism appears to be operative in these asymptomatic individuals, maintaining plasma steroid levels normal. The unbound fraction of T may be somewhat increased in overweight women with predominantly upper body fat deposition. The increased clearance of androgen may arise from an obesity-related depression in SHBG concentration (e.g., for T, E2, Δ5-diol, etc.). Adipose tissue, by virtue of the lipid solubility of most of these steroids, concentrates androgens, estrogens, and progesterone. This steroid sequestration not only contributes to the obesity-related increase in androgen clearance but also leads to an extremely enlarged total body steroid pool. Fat tissue sequestration also increases the concentration of androgens in the vicinity of adipose stromal cells, possibly encouraging their aromatization. Adipose tissue also has a moderate degree of 17-hydroxysteroid dehydrogenase activity, which appears to stimulate the conversion of A to T. Finally, alterations in peripheral and hepatic conjugation and an accelerated urinary excretion may contribute to the elevated clearance of androgens. The accelerated PR of androgens may simply result as compensation for the elevated MCR in obesity. Nonetheless, evidence of alteration(s) in adrenocortical steroidogenesis has been presented suggesting a selective obesity-related enhancement in adrenal androgen secretion. These remain to be confirmed. Nonetheless, adrenocortical abnormalities may arise secondary to the influence of other circulating and intra-adrenal factors, including insulin, prolactin, estrogens, and androgens. It is not known whether the accelerated androgen metabolism or the aberrant adrenal steroidogenesis improve with weight reduction. Excess body fat increases androgen aromatization which, together with an obesity-related decrease in SHBG, is associated with mildly elevated levels of E, and free E2 in postmenopausal women. Although premenopausal obese individuals have the same tendency, the far greater ovarian estrogen secretion overshadows any differences. The bulk of aromatization activity in fat lies in the stromal comportment. The major substrate for peripheral estrogen production is A. Testosterone also contributes to the estrogen pool via its conversion to E2. An increase in hepatic aromatization may also be present in obese individuals but remains to be clearly demonstrated. Weight reduction does not alter estrogen levels significantly, and the A-to-E1 conversion may actually increase. Sex hormone-binding globulin plasma concentrations and probably its hepatic production, are inversely correlated with body weight. The mechanism is not clear but may relate to the circulating androgen/estrogen ratio. The decreased SHBG levels are associated with higher free fractions of E2, T, Δ5-diol, and with an elevated MCR of bound steroids. The greater affinity of SHBG for T over E2 serves to amplify the effect of this estrogen on sensitive tissue. Sex hormone-binding globulin circulating levels normalize after weight loss. Obesity is associated with insulin resistance secondary to a decrease in receptor numbers, although postreceptor defects may also be present. In eumenorrheic individuals, the correlation between obesity, insulin resistance, and hyperandrogenemia is weak but appears to be stronger in women with upper body obesity. Individuals with a greater degree of upper body fat are also more susceptible to glucose/insulin and lipid abnormalities (male risk profile); although T levels may be positively associated with insulin resistance, DHA-S is probably not. Abnormalities in insulin/glucose homeostasis return to normal after weight loss. Gonadotropin secretion and control are not significantly different in obese women compared with normal weight subjects. Although abnormalities in the hypothalamic-pituitary control of PRL may be present in overweight individuals, circulating PRL levels remain normal. Accelerated MCR and PR of PRL are observed in obesity.