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Original Studies |
Division of Endocrinology, Diabetes, and Metabolism (S.D.-J.) and Department of Psychiatry (G.S., A.K.M., J.W.N.), Washington University School of Medicine, St. Louis, Missouri 63110
Address all correspondence and requests for reprints to: Samuel Dagogo-Jack, M.D., Division of Endocrinology, Diabetes, and Metabolism, Washington University School of Medicine, Box 8127, 660 South Euclid Avenue, St. Louis, Missouri 63110. E-mail: sdagogo{at}imgate.wustl.edu
Although leptin reverses obesity in rodents, its function and regulation in humans are unknown. Glucocorticoids have been reported to stimulate leptin production in both rodents and humans, but data assessing the effect of obesity on dynamic leptin secretory responses are unavailable. We, therefore, studied 52 lean and obese subjects [20 men and 32 women; aged 19–84 yr; body mass index (BMI) range, 16–47 kg/m2] randomized to treatment with dexamethasone (total dose, 10 mg/4 days) or placebo. Compared with placebo, dexamethasone increased (P = 0.0001) plasma leptin levels by 64–111% above baseline values within 2–4 days. The increases occurred in all ages, showed no sexual dimorphism, and were particularly robust in obese subjects. After dexamethasone treatment, significant interactions were observed between the change in plasma leptin and BMI (P = 0.0001), baseline plasma leptin (P = 0.0006) and plasma dexamethasone levels (P = 0.04), but not age (P = 0.28); an apparent interaction with plasma insulin no longer was significant after controlling for BMI. These results confirm dexamethasone-induced hyperleptinemia in humans and further demonstrate that the response is not defective in obesity.
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