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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Bibliografiska uppgifter
Huvudupphovsmän: Morgan, Stuart A., McCabe, Emma L., Gathercole, Laura L., Hassan-Smith, Zaki K., Larner, Dean P., Bujalska, Iwona J., Stewart, Paul M., Tomlinson, Jeremy W., Lavery, Gareth G.
Materialtyp: Artigo
Språk:Inglês
Publicerad: National Academy of Sciences 2014
Ämnen:
PNAS Plus
Länkar: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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