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  • Title: Serum leptin concentrations in patients with anorexia nervosa, bulimia nervosa and non-specific eating disorders correlate with the body mass index but are independent of the respective disease.
    Author: Ferron F, Considine RV, Peino R, Lado IG, Dieguez C, Casanueva FF.
    Journal: Clin Endocrinol (Oxf); 1997 Mar; 46(3):289-93. PubMed ID: 9156037.
    Abstract:
    OBJECTIVE: Leptin, the product of the ob gene, is a recently discovered hormone secreted by adipocytes. Serum leptin concentrations increase in correlation with the percentage of body fat, but little else is known about the physiological actions of leptin in humans. The aim of this study was to determine the role of leptin in severe eating disorders, and whether its levels are correlated with the specific disease or exclusively with body weight. TESTS: Serum concentrations of human leptin were analysed by specific radioimmunoassay and compared with the individual body mass indexes (BMI). The correlations between serum leptin concentrations and BMI, age and height were analysed. PATIENTS: A total of 65 women were studied: 25 patients with anorexia nervosa, 20 women with bulimia nervosa, 6 women with a diagnosis of nonspecific eating disorder, and 14 normal-weight women who acted as controls. At the time of the study, the patients were non-cured, under treatment, and at different stages of therapeutic evolution. MEASUREMENTS: Plasma leptin levels were measured by specific radioimmunoassay. RESULTS: The mean serum leptin in the normal-weight women was 10.5 +/- 1.1 micrograms/l, compared with 7.6 +/- 1.1 micrograms/l in the anorexia nervosa patients (P < 0.05). This reduction in leptin levels was paralleled by the differences in BMI (21.4 +/- 0.4 vs 18.8 +/- 0.2) P < 0.05. These differences between the controls and anorexia nervosa patients were not observed in patients with bulimia nervosa who had a mean serum leptin level of 9.9 +/- 1.4 micrograms/l and BMI of 21.3 +/- 0.6, neither significantly different from controls. On the contrary, patients with non-specific eating disorders showed a large reduction in BMI (17.9 +/- 1.2, P < 0.05 vs control), and a parallel reduction in serum leptin levels, 4.5 +/- 1.0 (P < 0.05 vs controls). When individual values of leptin were plotted against BMI a wide range was observed in all groups; in the control subjects from 5.6 to 17.7 micrograms/l, in anorexia nervosa patients from 2.1 to 28.1 micrograms/l, in patients with bulimia nervosa between 2.6 and 25.9 micrograms/l, and in women with non-specific eating disorder from 2.0 to 8.9. No correlation was observed with the specific disease but in each group a significant correlation was observed only with BMI. CONCLUSIONS: Serum leptin levels in three groups of patients affected by severe eating disorders are not related to the specific pathology but are correlated with the individual BMI. The analysis of leptin values may be a useful index of assessing the adipose tissue stores in the clinical setting, but will be of no help for diagnosis nor prognosis of severe eating disorders.
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