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11β-HSD1 is the major regulator of the tissue-specific effects of circulating glucocorticoid excess
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...
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Main Authors: | , , , , , , , , |
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Formato: | Artigo |
Idioma: | Inglês |
Publicado em: |
National Academy of Sciences
2014
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Assuntos: | |
Acesso em linha: | https://ncbi.nlm.nih.gov/pmc/articles/PMC4066483/ https://ncbi.nlm.nih.gov/pubmed/24889609 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1073/pnas.1323681111 |
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