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Inhibition of 11beta-hydroxysteroid dehydrogenase type 1 activity in vivo limits glucocorticoid exposure to human adipose tissue and decreases lipolysis.

Abstract:

CONTEXT: The pathophysiological importance of glucocorticoids (GCs) is exemplified by patients with Cushing's syndrome who develop hypertension, obesity, and insulin resistance. At a cellular level, availability of GCs to the glucocorticoid and mineralocorticoid receptors is controlled by the isoforms of 11beta-hydroxysteroid dehydrogenase (11beta-HSD). In liver and adipose tissue, 11beta-HSD1 converts endogenous, inactive cortisone to active cortisol but also catalyzes the bioactivation of t...

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Publication status:
Published

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Publisher copy:
10.1210/jc.2006-2325

Authors


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Institution:
University of Oxford
Department:
Oxford, MSD, RDM
Sherlock, M More by this author
Hughes, SV More by this author
Kilvington, F More by this author
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Journal:
The Journal of clinical endocrinology and metabolism
Volume:
92
Issue:
3
Pages:
857-864
Publication date:
2007-03-05
DOI:
EISSN:
1945-7197
ISSN:
0021-972X
URN:
uuid:8af5a540-4c6f-459f-b8e0-c250aadde678
Source identifiers:
482098
Local pid:
pubs:482098

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