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11β-HSD1 is the major regulator of the tissue-specific effects of circulating glucocorticoid excess.

Abstract:

The adverse metabolic effects of prescribed and endogenous glucocorticoid (GC) excess, Cushing syndrome, create a significant health burden. We found that tissue regeneration of GCs by 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1), rather than circulating delivery, is critical to developing the phenotype of GC excess; 11β-HSD1 KO mice with circulating GC excess are protected from the glucose intolerance, hyperinsulinemia, hepatic steatosis, adiposity, hypertension, myopathy, and dermal a...

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Publication status:
Published

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Publisher copy:
10.1073/pnas.1323681111

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Publisher:
National Academy of Sciences
Journal:
Proceedings of the National Academy of Sciences of the United States of America
Volume:
111
Issue:
24
Pages:
E2482-E2491
Publication date:
2014-06-01
DOI:
EISSN:
1091-6490
ISSN:
0027-8424
Source identifiers:
482050

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