title: Absence of exercise-induced leptin suppression associated with insufficient epinephrine reserve in patients with classic congenital adrenal hyperplasia due to 21-hydroxylase deficiency.
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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Division of Pediatric Endocrinology, Department of Pediatrics, Christian-Albrechts-Universität Kiel, Kiel, Germany. friepe@pediatrics.uni-kiel.de
authors.forename: F G
authors.initials: FG
authors.lastname: Riepe
authors.forename: N
authors.initials: N
authors.lastname: Krone
authors.forename: S N
authors.initials: SN
authors.lastname: Krüger
authors.forename: F C G J
authors.initials: FC
authors.lastname: Sweep
authors.forename: J W M
authors.initials: JW
authors.lastname: Lenders
authors.forename: J
authors.initials: J
authors.lastname: Dötsch
authors.forename: H
authors.initials: H
authors.lastname: Mönig
authors.forename: W G
authors.initials: WG
authors.lastname: Sippell
authors.forename: C-J
authors.initials: CJ
authors.lastname: Partsch
mesh_terms: D000293:Adolescent; D000312:Adrenal Hyperplasia, Congenital / Q000097:blood*; D000328:Adult; D001786:Blood Glucose; D004837:Epinephrine / Q000097:blood*; D015444:Exercise; D005260:Female; D006339:Heart Rate; D006801:Humans; D020738:Leptin / Q000097:blood*; D008297:Male
chemical_list: D001786:Blood Glucose; D020738:Leptin; D004837:Epinephrine