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

Journal article

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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Authors: Tomlinson, J; Sherlock, M; Hughes, B; Hughes, S; Kilvington, F

• Publication status: Published
• Journal: Journal of clinical endocrinology and metabolism
• Volume: 92
• Issue: 3
• Pages: 857-864
• Publication date: 2007-03-01
• DOI: 10.1210/jc.2006-2325
• EISSN: 1945-7197
• ISSN: 0021-972X
• Language: English
• Keywords: Extracellular Fluid; Carbenoxolone; Adipose Tissue; 11-beta-Hydroxysteroid Dehydrogenase Type 1; Prednisolone; Hydrocortisone; Humans; Serum; Adult; Male; Glucocorticoids; Lipolysis