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Reduced 11ß-hydroxysteroid dehydrogenase type 1 activity in obese boys

¹ Paediatric Endocrinology, Campus Virchow, Charité University Medicine Berlin, 13353 Berlin, Germany, ² Clinical Endocrinology, Charité Campus Mitte, Charité University Medicine Berlin, Charitéplatz 1, D 10117 Berlin, Germany, ³ Department of Nutrition and Health, Research Institute of Child Nutrition, 44225 Dortmund, Germany, ⁴ Steroid Research Unit, Center of Child and Adolescent Medicine, Justus Liebig University, 35392 Giessen, Germany and ⁵ Division of Medical Sciences, Institute of Biomedical Research, University of Birmingham, Queen Elizabeth Hospital, Birmingham, B15 2TH, UK

(Correspondence should be addressed to M Quinkler; Email: marcus.quinkler{at}charite.de)

Objective: The incidence of childhood obesity and type 2 diabetes has reached epidemic proportions. Glucocorticoid excess causes central obesity and diabetes mellitus as seen in Cushing’s syndrome. The 11ß-hydroxysteroid dehydrogenase type 1 enzyme (11ß-HSD1) regenerates active cortisol from inactive cortisone. Altered 11ß-HSD1 may cause tissue-specific Cushing’s syndrome with central obesity and impaired glucose homeostasis.

Design, patients, and methods: Clinical and laboratory characteristics, and anthropometric measurements were determined in 15 male and 6 female obese pubertal children (aged 12–18 years, Tanner stages 2–5). In addition, analyses of 24-h excretion rates of glucocorticoids were also performed in 21 age-, sex-, and pubertal stage-matched non-obese children using gas chromatographic–mass spectrometric (GC–MS) analysis.

Results: 11ß-HSD1 activity (urinary tetrahydrocortisol (THF) + 5-THF/tetrahydrocortisone (THE) ratio) was lower in obese when compared with non-obese boys. In addition, obese children had a higher total cortisol metabolite excretion than non-obese children. 11ß-HSD1 activity was significantly related to age in lean and obese children. Standard deviation score (SDS)-body mass index did not correlate with 11ß-HSD1 activity, or with total cortisol metabolite excretion within each group. In obese children, 11ß-HSD1 activity and total cortisol metabolite excretion showed no correlation to waist-to-hip ratio, fat mass (percentage of body mass), or the homeostasis model assessment of insulin resistance index.

Conclusions: In conclusion, our findings strongly suggest that 11ß-HSD1 activity increases with age, and is reduced in obese boys. In addition, obese children have a higher total cortisol metabolites excretion suggesting a stimulated hypothalamus–pituitary–adrenal axis.