z-logo
open-access-imgOpen Access
Changes in Adenosine 5′-Monophosphate-Activated Protein Kinase as a Mechanism of Visceral Obesity in Cushing’s Syndrome
Author(s) -
Blerina Kola,
Mirjam ChristCrain,
Francesca Lolli,
Giorgio Arnaldi,
Gilberta Giacchetti,
Marco Boscaro,
Ashley Grossman,
Márta Korbonits
Publication year - 2008
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.2008-1297
Subject(s) - medicine , endocrinology , adipose tissue , ampk , metabolic syndrome , insulin resistance , glucocorticoid , abdominal obesity , protein kinase a , biology , insulin , kinase , obesity , microbiology and biotechnology
Features of the metabolic syndrome such as central obesity with insulin resistance and dyslipidemia are typical signs of Cushing's syndrome and common side effects of prolonged glucocorticoid treatment. AMP-activated protein kinase (AMPK), a key regulatory enzyme of lipid and carbohydrate metabolism as well as appetite, is involved in the development of the deleterious metabolic effects of excess glucocorticoids, but no data are available in humans. In the current study, we demonstrate the effect of high glucocorticoid levels on AMPK activity of human adipose tissue samples from patients with Cushing's syndrome.

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