Circulating Sclerostin Levels Are Decreased in Patients with Endogenous Hypercortisolism and Increase after Treatment
Author(s) -
Antoon H van Lierop,
Anke W. van der Eerden,
Neveen A. T. Hamdy,
A. R. M. M. Hermus,
Martin den Heijer,
Socrates E. Papapoulos
Publication year - 2012
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.2012-2218
Subject(s) - sclerostin , n terminal telopeptide , endocrinology , medicine , endogeny , procollagen peptidase , bone remodeling , adrenalectomy , chemistry , alkaline phosphatase , osteocalcin , wnt signaling pathway , biochemistry , gene , enzyme
Increased bone fragility is a frequent complication of hypercortisolism due predominantly to suppression of bone formation. Sclerostin is an osteocyte-produced negative regulator of bone formation, which is up-regulated by glucocorticoids in mice.
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