Exp Clin Endocrinol Diabetes 2003; 111(5): 278-282
DOI: 10.1055/s-2003-41286
Article

J. A. Barth Verlag in Georg Thieme Verlag Stuttgart · New York

Serum Leptin Monitoring in Anorectic Patients During Refeeding Therapy

S. Lob 1 , J. Pickel 1 , M. Bidlingmaier 2 , L. Schaaf 1 , H. Backmund 1 , M. Gerlinghoff 1 , G. K. Stalla 1
  • 1Max-Planck-Institute of Psychiatry, Munich, Germany
  • 2Klinikum Innenstadt, LMU Munich, Germany
Weitere Informationen

Publikationsverlauf

Received: July 31, 2002 First decision: October 20, 2002

Accepted: January 10, 2003

Publikationsdatum:
02. September 2003 (online)

Abstract

Circulating concentrations of leptin are exceedingly low in severe malnutrition as seen in the acute state of anorexia nervosa (AN). During refeeding therapy plasma leptin levels increase to normal and in some cases peak at values in excess of the BMI of matched controls even before a normal body weight has been achieved. Peak leptin levels are possibly the cause of an increased energy expenditure during this stage of the disorder and might predispose to renewed weight loss (rebound phenomenon). In this study we investigated the role of leptin fluctuations as a prognostic factor of therapeutic success in AN. In 11 anorectic female patients serum leptin levels, BMI and body fat percentage were evaluated in four-week intervals during a conventional refeeding program over three months (group 1). The results of the first two measurements were used to determine a range of increases in leptin levels in relation to increases in BMI. The values between the 25th and 75th percentiles determined the reference range. In a second group of 9 anorectic female patients serum leptin levels, BMI, body fat percentage and the increase in the leptin level in relation to the BMI of each subject were investigated for three months every two weeks. These patients were also treated according to the same conventional refeeding program, but the caloric intake was reduced or increased (± 250 kcal/d) if the increase in the leptin level, in relation to the increase in the BMI, had exceeded or fallen short of the reference range. During the refeeding therapy every subject of each group experienced increases in serum leptin levels, BMI and body fat percentage. Six subjects of group 1 and six subjects of the second group had an increase in leptin levels in relation to the increase of the BMI out of the reference range at least once. To investigate the therapeutic outcome of leptin monitoring and the following alteration of caloric intake, weight gain of the patients of both groups during the whole treatment was compared. No significant difference was found. Our results probably do not support the findings that high leptin levels predispose to a renewed loss of weight. The outcome in our patients whose caloric intake was modified due to their serum leptin levels was not significantly improved.

References

  • 1 Blum W F, Englaro P, Hanitsch S, Juul A, Hertel N T, Müller J, Skakkebaek N E, Heiman M L, Birkett M, Attanasio A M, Kiess W, Rascher W. Plasma leptin levels in healthy children and adolescents: dependence on body mass index, body fat mass, gender, pubertal stage and testosterone.  J Clin Endocrinol Metab. 1997;  82 2904-2910
  • 2 Caro J F, Sinha M K, Kolaczynski J W, Zhang P, Considine R V. Leptin: The tale of an obesity gene.  Diabetes. 1996;  45 1455-1462
  • 3 Hebebrand J, Blum W F, Barth N, Coners H, Englaro P, Juul A, Ziegler A, Warnke A, Rascher W, Remschmidt H. Leptin levels in patients with anorexia nervosa are reduced in the acute stage and elevated upon short-term weight restoration.  Mol Psychiatry. 1997;  2 330-334
  • 4 Hebebrand J, van der Heyden J, Devos R, Köpp W, Herpertz S, Remschmidt H, Herzog W. Plasma concentrations of obese protein in anorexia nervosa.  Lancet. 1995;  346 1624-1625
  • 5 Herpertz S, Albers N, Wagner R, Pelz B, Köpp W, Mann K, Blum W F, Senf W, Hebebrand J. Longitudinal changes of circadian leptin, insulin and cortisol plasma levels and their correlation during refeeding in patients with anorexia nervosa.  Eur J Endocrinol. 2000;  142 373-379
  • 6 Kolaczynski J W, Considine R V, Ohannasian J P, Marco C C, Opentanova I, Nyce M R, Myint M, Caro J F. Responses to leptin to short-term fasting and refeeding in humans: a link with ketogenesis but not ketones themselves.  Diabetes. 1996 a;  45 1511-1515
  • 7 Kolaczynski J W, Ohannesian J P, Considine R V, Marco C C, Caro J F. Response of leptin to short-term and prolonged overfeeding in humans.  J Clin Endocrinol Metab. 1996 b;  81 4162-4165
  • 8 Lear S A, Pauly R P, Birmingham C L. Body fat, caloric intake, and plasma leptin levels in women with anorexia nervosa.  Int J Eat Disord. 1997;  26 283-288
  • 9 Mantzoros C S, Flier J S, Lesem M D, Brewerton T D, Jimerson D C. Cerebrospinal fluid leptin in anorexia nervosa: correlation with nutritional status and potential role in resistance to weight gain.  J Clin Endocrinol Metab. 1997;  82 1845-1851
  • 10 Monteleone P, Fabrazzo M, Tortorella A, Fuschino A, Maj M. Opposite modifications in circulating leptin and soluble leptin receptor across the eating disorder spectrum.  Mol Psychiatry. 2002;  7 641-646
  • 11 Polito A, Fabbri A, Ferro-Luzzi A, Cuzzolaro M, Censi L, Ciarapica D, Fabbrini E, Giannini D. Basal metabolic rate in anorexia nervosa: relation to body composition and leptin concentrations.  Am J Clin Nutr. 2000;  71 1495-1502
  • 12 Wu Z, Bidlingmaier M, Liu C, De Souza E B, Tschöp M, Morrison K M, Strasburger C J. Quantification of the soluble leptin receptor in human blood by ligand-mediated immunofunctional assay.  J Clin Endocrinol Metab. 2002;  87 2931-2939
  • 13 Zhang Y, Proenca R, Maffei M, Barone M, Leopold L, Friedman J M. Positional cloning of the mouse obese gene and its human homologue.  Nature. 1994;  372 425-432

Simone Lob

Max-Planck-Institut für Psychiatrie, München
Arbeitsgruppe Endokrinologie

Kraepelinstraße 2

80804 München

Germany

Telefon: + 498953849553

eMail: simone.lob@stud.uni-muenchen.de