Reduced 11beta-hydroxysteroid dehydrogenase type 1 activity in obese boys.

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 11beta-hydroxysteroid dehydrogenase type 1 enzyme (11beta-HSD1) regenerates active cortisol...

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Main Authors: Wiegand, S, Richardt, A, Remer, T, Wudy, SA, Tomlinson, J, Hughes, B, Grüters, A, Stewart, P, Strasburger, C, Quinkler, M
Format: Journal article
Language:English
Published: 2007
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author Wiegand, S
Richardt, A
Remer, T
Wudy, SA
Tomlinson, J
Hughes, B
Grüters, A
Stewart, P
Strasburger, C
Quinkler, M
author_facet Wiegand, S
Richardt, A
Remer, T
Wudy, SA
Tomlinson, J
Hughes, B
Grüters, A
Stewart, P
Strasburger, C
Quinkler, M
author_sort Wiegand, S
collection OXFORD
description 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 11beta-hydroxysteroid dehydrogenase type 1 enzyme (11beta-HSD1) regenerates active cortisol from inactive cortisone. Altered 11beta-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: 11beta-HSD1 activity (urinary tetrahydrocortisol (THF) + 5alpha-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. 11beta-HSD1 activity was significantly related to age in lean and obese children. Standard deviation score (SDS)-body mass index did not correlate with 11beta-HSD1 activity, or with total cortisol metabolite excretion within each group. In obese children, 11beta-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 11beta-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.
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spelling oxford-uuid:30b81138-450e-4a5a-9ea5-496e068025ce2022-03-26T13:03:16ZReduced 11beta-hydroxysteroid dehydrogenase type 1 activity in obese boys.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:30b81138-450e-4a5a-9ea5-496e068025ceEnglishSymplectic Elements at Oxford2007Wiegand, SRichardt, ARemer, TWudy, SATomlinson, JHughes, BGrüters, AStewart, PStrasburger, CQuinkler, M 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 11beta-hydroxysteroid dehydrogenase type 1 enzyme (11beta-HSD1) regenerates active cortisol from inactive cortisone. Altered 11beta-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: 11beta-HSD1 activity (urinary tetrahydrocortisol (THF) + 5alpha-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. 11beta-HSD1 activity was significantly related to age in lean and obese children. Standard deviation score (SDS)-body mass index did not correlate with 11beta-HSD1 activity, or with total cortisol metabolite excretion within each group. In obese children, 11beta-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 11beta-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.
spellingShingle Wiegand, S
Richardt, A
Remer, T
Wudy, SA
Tomlinson, J
Hughes, B
Grüters, A
Stewart, P
Strasburger, C
Quinkler, M
Reduced 11beta-hydroxysteroid dehydrogenase type 1 activity in obese boys.
title Reduced 11beta-hydroxysteroid dehydrogenase type 1 activity in obese boys.
title_full Reduced 11beta-hydroxysteroid dehydrogenase type 1 activity in obese boys.
title_fullStr Reduced 11beta-hydroxysteroid dehydrogenase type 1 activity in obese boys.
title_full_unstemmed Reduced 11beta-hydroxysteroid dehydrogenase type 1 activity in obese boys.
title_short Reduced 11beta-hydroxysteroid dehydrogenase type 1 activity in obese boys.
title_sort reduced 11beta hydroxysteroid dehydrogenase type 1 activity in obese boys
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