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Original Studies |
Department of Psychiatry, University of Minnesota (E.D.E., N.R., P.T.), Minneapolis, Minnesota 55455; the Department of Internal Medicine, University of Kentucky (C.P.), Lexington, Kentucky 40536; and the Department of Medicine and General Clinical Research Center, Tulane University (P.F.K., C.Y.B.), New Orleans, Louisiana 70112
Address all correspondence and requests for reprints to: Elke D. Eckert, M.D., Department of Psychiatry, University of Minnesota Hospital, Box 393, Mayo Building, Minneapolis, Minnesota 55455.
Serum leptin levels are low in untreated anorexia nervosa, but studies of the exact relationship between leptin and body weight and the impact of refeeding in anorectics are limited. Therefore, we studied serum leptin, insulin-like growth factor I, and other endocrine parameters in female anorectics before and after gaining weight and in female normal body weight controls. Leptin levels in untreated anorectics were significantly lower than those in normal body weight controls (3.6 ± 1.6 vs. 12.0 ± 6.9 ng/mL; P < 0.001), and they uncoupled from body weight in a nonlinear relationship, suggesting a threshold effect at lowest body weights. Leptin increased significantly with refeeding (5.6 ±3.8 ng/mL; P < 0.01). The significant linear correlations of leptin with body mass index in the anorectics after weight gain and in normal body weight controls (r = 0.69; P < 0.001 and r = 0.76; P < 0.001, respectively) are consistent with a normal physiological increase in leptin with weight gain. Leptin and insulin-like growth factor I were highly correlated, even after controlling for body weight (r = 0.63; P = 0.001) during starvation, but were no longer significantly correlated after body weight gain in the anorectics or the normal body weight controls. Further studies are necessary to elucidate the relationship of leptin to neuroendrocrine abnormalities seen in starvation and to determine a possible contribution of leptin to difficulties with weight restoration in anorexia nervosa.
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