Dose-dependent cortisol-induced increases in plasma leptin concentration in healthy humans.

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Abstract
GLUCOCORTICOIDS (GCs) are the product of a stress-responsive hypothalamic-pituitary-adrenal axis, which has been implicated1,2 in the regulation of appetite and body weight. Research has been stimulated by identification of the mouse obese (ob) gene and its human homologue,3 mutation of which in the mouse produces obesity. The ob gene product, leptin, can induce weight loss by decreasing food intake and increasing metabolic activity.3-6 In humans, as in mice, leptin is secreted by adipocytes,7-10 with plasma leptin levels highly correlated with total body adiposity.8,11,12 Other factors regulating leptin levels in rodents include insulin, β-adrenergic agonists, and GCs,13-17 with the latter increasing ob messenger RNA synthesis and leptin secretion and decreasing food intake.15,16 In humans, the regulation18-20 and metabolism21 of leptin is less clear.