z-logo
open-access-imgOpen Access
Genetic Variation in 11β-Hydroxysteroid Dehydrogenase Type 1 Predicts Adrenal Hyperandrogenism among Lean Women with Polycystic Ovary Syndrome
Author(s) -
Alessandra Gambineri,
Valentina Vicennati,
Silvia Genghini,
Federica Tomassoni,
Uberto Pagotto,
Renato Pasquali,
Brian R. Walker
Publication year - 2006
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.2005-2222
Subject(s) - endocrinology , medicine , polycystic ovary , hyperandrogenism , dehydroepiandrosterone sulfate , androgen , obesity , dehydroepiandrosterone , cortisone , context (archaeology) , glucocorticoid , biology , hormone , insulin resistance , paleontology
Elevated adrenal androgen levels are common in polycystic ovary syndrome (PCOS), but the underlying pathogenetic mechanism is poorly understood. In the rare cortisone reductase deficiency, impaired regeneration of active cortisol from inert cortisone by 11beta-hydroxysteroid dehydrogenase (11beta-HSD1) results in compensatory activation of ACTH secretion and adrenal hyperandrogenism. 11beta-HSD1 deficiency may protect against obesity and its metabolic consequences because of impaired regeneration of cortisol in adipose tissue.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.
Having issues? You can contact us here
Accelerating Research

Address

John Eccles House
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom