Reduced 11β-hydroxysteroid dehydrogenase type 1 activity in obese boys
Author(s) -
Susanna Wiegand,
Anna Richardt,
Thomas Remer,
Stefan A. Wudy,
Jeremy Tomlinson,
Beverly Hughes,
Annette Grüters,
Paul M. Stewart,
Christian J. Strasburger,
Marcus Quinkler
Publication year - 2007
Publication title -
european journal of endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.897
H-Index - 148
eISSN - 1479-683X
pISSN - 0804-4643
DOI - 10.1530/eje-07-0193
Subject(s) - medicine , endocrinology , 11β hydroxysteroid dehydrogenase type 1 , cortisone , obesity , body mass index , excretion , metabolite , glucocorticoid , insulin resistance , chemistry , dehydrogenase , enzyme , biochemistry
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.
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