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Exp Clin Endocrinol Diabetes 2006; 114(3): 105-110
DOI: 10.1055/s-2005-865836
Article

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

Absence of Exercise-Induced Leptin Suppression Associated with Insufficient Epinephrine Reserve in Patients with Classic Congenital Adrenal Hyperplasia Due to 21-Hydroxylase Deficiency

F. G. Riepe1 , N. Krone1 , S. N. Krüger1 , F. C. G. J. Sweep2 , J. W. M. Lenders2 , J. Dötsch3 , H. Mönig4 , W. G. Sippell1 , C.-J. Partsch5
  • 1Division of Pediatric Endocrinology, Department of Pediatrics, Christian-Albrechts-Universität Kiel, Kiel, Germany
  • 2Departments of Chemical Endocrinology and Internal Medicine, University Medical Center Nijmegen, Nijmegen, The Netherlands
  • 3Department of Pediatrics, Friedrich-Alexander Universität Erlangen, Erlangen, Germany
  • 41st Department of Internal Medicine, Christian-Albrechts-Universität Kiel, Kiel, Germany
  • 5Children's Hospital, Städtische Kliniken Esslingen, Esslingen, Germany
Further Information

Publication History

Received: September 19, 2004 First decision: May 13, 2005

Accepted: June 22, 2005

Publication Date:
25 April 2006 (online)

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Abstract

Objective: Patients with congenital adrenal hyperplasia (CAH) due to 21-hydroxylase deficiency suffer from glucocorticoid and mineralocorticoid deficiency. They have insufficient epinephrine reserves and increased basal leptin levels and are often insulin resistant. In healthy subjects, an inhibitory effect of acute catecholamine elevation on the leptin plasma concentrations has been reported. However, it is not yet known how leptin levels respond to exercise in CAH patients. Methods: We performed a cycle ergometer test in six CAH patients to measure the response of plasma leptin, glucose and the catecholamines, epinephrine (E) and norepinephrine (N), as well as their respective metabolites, metanephrine (M) and normetanephrine (NM), to intense exercise. Results: Baseline leptin concentrations in CAH patients were not different from those of controls. Leptin levels decreased significantly with exercise in healthy controls, whereas they remained unchanged in CAH patients. In contrast to controls, CAH patients showed no rise of plasma glucose. Basal and stimulated E and M levels were significantly lower in CAH patients compared to controls. Baseline and stimulated N and NM levels were comparable, showing a significant rise after exercise. Peak systolic blood pressure and peak heart rate in both groups were comparable. Conclusion: CAH patients do not manifest exercise-induced leptin suppression. The most probable reason for this is their severely impaired epinephrine stress response. In addition, epinephrine deficiency is leading to secondary changes in various catecholamine dependent metabolic pathways, e. g., energy balance. Although obvious clinical sequelae are so far unknown, the catecholamine-deficient state and the resulting hyperleptinemia might contribute to the severity of the disease in CAH.

Key words

Congenital adrenal hyperplasia - leptin - physical exercise

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Dr. med. Felix G. Riepe

Department of Pediatrics
Christian-Albrechts-University of Kiel

Schwanenweg 20

24105 Kiel

Germany

Phone: + 494315971622

Fax: + 49 43 15 97 18 31

Email: friepe@pediatrics.uni-kiel.de

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