The Role of 11ß-Hydroxysteroid Dehydrogenase 1 in Adipogenesis in Thyroid-Associated Ophthalmopathy
Author(s) -
Jeremy Tomlinson,
Omar M. Durrani,
Iwona Bujalska,
Laura Gathercole,
Paul J. Tomlins,
Tristan T. Q. Reuser,
Geoffrey E. Rose,
John Curnow,
Paul M. Stewart,
Elizabeth A. Walker,
Saaeha Rauz
Publication year - 2009
Publication title -
the journal of clinical endocrinology and metabolism
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.206
H-Index - 353
eISSN - 1945-7197
pISSN - 0021-972X
DOI - 10.1210/jc.2009-0873
Subject(s) - medicine , endocrinology , glucocorticoid , adipogenesis , stromal cell , adipose tissue , glucocorticoid receptor , inflammation , proinflammatory cytokine , dehydrogenase , adipocyte , biology , chemistry , enzyme , biochemistry
Thyroid-associated ophthalmopathy (TAO) is a sight-threatening autoimmune disease in which de novo adipogenesis has been identified as a fundamental pathogenic mechanism. 11beta-Hydroxysteroid dehydrogenase 1 (11beta-HSD1) increases cortisol bioavailability and is pivotal in mediating glucocorticoid responses in adipose tissue and inflammation.
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