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Reproductive Endocrinology |
United States Department of Agriculture/Agricultural Research Service Children’s Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine (N.F.B., J.M.H.), Houston, Texas 77030; and Amgen Incorporated (M.A.N.), Thousand Oaks, California 91320
Address all correspondence and requests for reprints to: Nancy F. Butte, Children’s Nutrition Research Center, Baylor College of Medicine, 1100 Bates Street, Houston, Texas 77030.
Experiments in ob/ob female mice demonstrated that leptin injections not only reduced weight and fat mass, but also restored fertility and partial lactation. To explore factors regulating ob gene expression in reproductive women, we measured serum leptin, body fat, energy expenditure, and milk production in 65 women at 36 weeks of gestation, and at 3 and 6 months postpartum. Serum leptin was measured by solid-phase sandwich enzyme immunoassay, and serum insulin and PRL by solid-phase 125I RIA. Total body water by deuterium dilution, body volume by hydrodensitometry, and bone density by dual-energy x-ray absorptiometry were used to estimate body fat. Serum leptin per unit fat mass was significantly higher at 36 weeks of pregnancy than at 3 and 6 months postpartum (1.25 vs. 0.75, 0.73 ng·mL-1·kg-1). Postpartum normalization of leptin was associated with changes not only in weight and fat mass, but also serum insulin. Leptin was not different between lactating and nonlactating women. Leptin may have affected milk production indirectly through its negative effect on serum PRL. Adjusted for fat-free mass and fat mass, rates of energy expenditure were not significantly correlated with leptin. Our results provide evidence that factors other than fat mass alone modulate serum leptin in reproductive women.
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