Inhibition of 11β-Hydroxysteroid Dehydrogenase Type 1 Activity in Vivo Limits Glucocorticoid Exposure to Human Adipose Tissue and Decreases Lipolysis | Zendy

Jeremy Tomlinson | Zendy; Mark Sherlock | Zendy; B. Hughes | Zendy; Susan V. Hughes | Zendy; Fiona Kilvington | Zendy; William A. Bartlett | Zendy; Rachel Courtney | Zendy; Paul A. Rejto | Zendy; William W. Carley | Zendy; Paul M. Stewart | Zendy

Open Access

Inhibition of 11β-Hydroxysteroid Dehydrogenase Type 1 Activity in Vivo Limits Glucocorticoid Exposure to Human Adipose Tissue and Decreases Lipolysis

Author(s) -

Jeremy Tomlinson,

Mark Sherlock,

B. Hughes,

Susan V. Hughes,

Fiona Kilvington,

William A. Bartlett,

Rachel Courtney,

Paul A. Rejto,

William W. Carley,

Paul M. Stewart

Publication year - 2007

Publication title -

the journal of clinical endocrinology and metabolism

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.206

H-Index - 353

eISSN - 1945-7197

pISSN - 0021-972X

DOI - 10.1210/jc.2006-2325

Subject(s) - endocrinology , medicine , adipose tissue , lipolysis , glucocorticoid , cortisone , microdialysis , prednisolone , chemistry , 11β hydroxysteroid dehydrogenase type 1 , dehydrogenase , biochemistry , enzyme , central nervous system

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 the synthetic prednisone to prednisolone.

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