| http://purl.uniprot.org/citations/24889609 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/24889609 | http://www.w3.org/2000/01/rdf-schema#comment | "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 atrophy of Cushing syndrome. Whereas liver-specific 11β-HSD1 KO mice developed a full Cushingoid phenotype, adipose-specific 11β-HSD1 KO mice were protected from hepatic steatosis and circulating fatty acid excess. These data challenge our current view of GC action, demonstrating 11β-HSD1, particularly in adipose tissue, is key to the development of the adverse metabolic profile associated with circulating GC excess, offering 11β-HSD1 inhibition as a previously unidentified approach to treat Cushing syndrome."xsd:string |
| http://purl.uniprot.org/citations/24889609 | http://purl.org/dc/terms/identifier | "doi:10.1073/pnas.1323681111"xsd:string |
| http://purl.uniprot.org/citations/24889609 | http://purl.uniprot.org/core/author | "Stewart P.M."xsd:string |
| http://purl.uniprot.org/citations/24889609 | http://purl.uniprot.org/core/author | "Bujalska I.J."xsd:string |
| http://purl.uniprot.org/citations/24889609 | http://purl.uniprot.org/core/author | "Lavery G.G."xsd:string |
| http://purl.uniprot.org/citations/24889609 | http://purl.uniprot.org/core/author | "Tomlinson J.W."xsd:string |
| http://purl.uniprot.org/citations/24889609 | http://purl.uniprot.org/core/author | "Gathercole L.L."xsd:string |
| http://purl.uniprot.org/citations/24889609 | http://purl.uniprot.org/core/author | "Hassan-Smith Z.K."xsd:string |
| http://purl.uniprot.org/citations/24889609 | http://purl.uniprot.org/core/author | "Morgan S.A."xsd:string |
| http://purl.uniprot.org/citations/24889609 | http://purl.uniprot.org/core/author | "McCabe E.L."xsd:string |
| http://purl.uniprot.org/citations/24889609 | http://purl.uniprot.org/core/author | "Larner D.P."xsd:string |
| http://purl.uniprot.org/citations/24889609 | http://purl.uniprot.org/core/date | "2014"xsd:gYear |
| http://purl.uniprot.org/citations/24889609 | http://purl.uniprot.org/core/name | "Proc Natl Acad Sci U S A"xsd:string |
| http://purl.uniprot.org/citations/24889609 | http://purl.uniprot.org/core/pages | "E2482-91"xsd:string |
| http://purl.uniprot.org/citations/24889609 | http://purl.uniprot.org/core/title | "11beta-HSD1 is the major regulator of the tissue-specific effects of circulating glucocorticoid excess."xsd:string |
| http://purl.uniprot.org/citations/24889609 | http://purl.uniprot.org/core/volume | "111"xsd:string |
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