Correlation between estrogens and serum adipocytokines in premenopausal and postmenopausal women

Objective: The purpose of this study was to investigate the association between serum adipocytokines (adiponectin, resistin, leptin, and tumor necrosis factor alpha [TNF-alpha]) and endogenous estrogen (estrone and estradiol) levels in healthy premenopausal and postmenopausal women. Design: This study included 53 healthy premenopausal women, 45 healthy postmenopausal women, and 10 postmenopausal women with the metabolic syndrome who were participating in general health examinations. A secondary analysis was performed on levels of adiponectin, resistin, leptin, TNF-ot, estrone (E-1), and estradiol (E-2). Results: After accounting for body mass index, TNF-ot was significantly increased (1.5 +/- 0.1 vs 2.0 +/- 0.1 pg/mL, P < 0.05) in healthy postmenopausal women as compared with healthy premenopausal women, whereas leptin was decreased (5.6 +/- 1.1 vs 4.0 +/- 1.1 ng/mL). Estrogen (E-1 and E-2) was positively correlated with leptin in only healthy premenopausal women, whereas estrogen did not correlate with any adipocytokine in healthy postmenopausal women. In the multiple regression analysis, only leptin significantly contributed to insulin resistance. Combining healthy premenopausal and postmenopausal women, El correlated negatively with TNF-alpha (r = -0.23, P < 0.05) and positively with leptin (r = 0.35, P < 0.01) and did not correlate with resistin. E-2 correlated negatively with TNF-alpha (r = -0.24, P < 0.05) and positively with leptin (r = 0.34, P < 0.01); it did not correlate with adiponectin or resistin. Leptin might stimulate the increase of plasma gonadotropin-releasing hormone levels, which could result in a positive correlation with estrogen in premenopausal women but not in postmenopausal women. Conclusions: Estrogen deficiency resulted in increased TNF-ot levels. Serum leptin levels correlated positively with estrogen levels in premenopausal women. However, the increase in obesity in postmenopausal women increased leptin, which increases insulin resistance.