Abstract | OBJECTIVE: METHODS: 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.
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Authors | F G Riepe, N Krone, S N Krüger, F C G J Sweep, J W M Lenders, J Dötsch, H Mönig, W G Sippell, C-J Partsch |
Journal | Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association
(Exp Clin Endocrinol Diabetes)
Vol. 114
Issue 3
Pg. 105-10
(Mar 2006)
ISSN: 0947-7349 [Print] Germany |
PMID | 16636975
(Publication Type: Journal Article)
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Chemical References |
- Blood Glucose
- Leptin
- Epinephrine
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Topics |
- Adolescent
- Adrenal Hyperplasia, Congenital
(blood)
- Adult
- Blood Glucose
- Epinephrine
(blood)
- Exercise
- Female
- Heart Rate
- Humans
- Leptin
(blood)
- Male
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