Journal article
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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Authors
Bibliographic Details
- 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
Item Description
- Language:
- English
- Keywords:
- Pubs id:
-
pubs:482050
- UUID:
-
uuid:1b73d317-f52e-46bb-8649-ead7802ec35c
- Local pid:
- pubs:482050
- Deposit date:
- 2014-08-29
Terms of use
- Copyright date:
- 2014
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