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Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, the Netherlands
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Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, the Netherlands
Corcept Therapeutics, Menlo Park, CA, USA
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Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, the Netherlands
Corcept Therapeutics, Menlo Park, CA, USA
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gland ( Spencer & Deak 2017 ). Dysregulation of GC secretion is responsible for several pathologies, the most obvious being Cushing’s syndrome (CS). Endogenous CS is a condition characterized by cortisol overproduction that can be ACTH-dependent, caused
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Institute of Biomedicine, University of Barcelona, Barcelona, Spain
Centro de Investigación Biomédica en Red de Obesidad y Nutrición (CIBEROBN), Carlos III Health Institute, Madrid, Spain
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Institute of Biomedicine, University of Barcelona, Barcelona, Spain
Centro de Investigación Biomédica en Red de Obesidad y Nutrición (CIBEROBN), Carlos III Health Institute, Madrid, Spain
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Department of Endocrinology and Nutrition, Hospital Clinic of Barcelona, Barcelona, Spain
Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Carlos III Health Institute, Madrid, Spain
Department of Medicine, Faculty of Medicine and Health Sciences, University of Barcelona, Barcelona, Spain
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Introduction Chronic exposure to excess glucocorticoid (GC) levels, resulting from either endogenous Cushing’s syndrome (CS) or exogenous GC therapy, causes several adverse outcomes, including obesity, insulin resistance, dyslipidemia
Centre for Endocrinology Diabetes and Metabolism, Birmingham Health Partners, University of Birmingham, Birmingham, UK
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Centre for Endocrinology Diabetes and Metabolism, Birmingham Health Partners, University of Birmingham, Birmingham, UK
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Centre for Endocrinology Diabetes and Metabolism, Birmingham Health Partners, University of Birmingham, Birmingham, UK
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Centre for Endocrinology Diabetes and Metabolism, Birmingham Health Partners, University of Birmingham, Birmingham, UK
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Centre for Endocrinology Diabetes and Metabolism, Birmingham Health Partners, University of Birmingham, Birmingham, UK
School of Medicine, Worsley Building, University of Leeds, Leeds, UK
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Centre for Endocrinology Diabetes and Metabolism, Birmingham Health Partners, University of Birmingham, Birmingham, UK
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Introduction The pathophysiological effects of glucocorticoids (GCs) are well described and impact upon almost all organ systems within the body. This is highlighted in patients with GC excess, Cushing’s syndrome, characterized by central
Department of Biosciences, Nottingham Trent University, Nottingham, UK
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NEXUS, Discovery Way, University of Leeds, Leeds, UK
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Department of Biosciences, Nottingham Trent University, Nottingham, UK
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improve healthspan. Interestingly, the aged phenotype shares several metabolic similarities with that of circulatory glucocorticoid (GC) excess (Cushing’s syndrome), including insulin resistance, type 2 diabetes mellitus, central obesity, hypertension
Centre for Systems Health and Integrated Metabolic Research, Department of Biosciences, Nottingham Trent University, Birmingham, UK
Institute of Metabolism and Systems Research, University of Birmingham, Birmingham, UK
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Centre for Cardiovascular Science, University of Edinburgh, Edinburgh, UK
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dysfunction, most notably Cushing’s syndrome, which is characterised by a well-documented phenotype in humans and rodents ( Lacroix et al. 2015 , Lonser et al. 2017 ). This phenotype, which can be readily induced in mice for experimental purposes
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first sign of CVD in Cushing’s syndrome ( Isidori et al. 2015 a ), and patients with mild autonomous cortisol secretion exhibit increased arterial stiffness and cardiac remodeling ( Sbardella et al. 2018 ). Even though an exhaustive discussion of
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. There are compelling evidence to support elevated expression of certain G-protein-coupled receptors (GPCRs) as a cause of some cases of adrenocorticotrophin (ACTH)-independent Cushing’s syndrome ( Bugalho et al. 2000 , Dall’Asta et al. 2004
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administration and the risk to induce long-term adverse effects. Recently, a case of acute iatrogenic Cushing’s syndrome and HPA axis suppression which persisted 8 months has been reported in humans after a single-dose i.m. depot TAA administration ( Iglesias et
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consequently produces mineralocorticoids. CYP17 dysfunction has been associated with a number of diseases including polycystic ovary syndrome ( Qin & Rosenfield 1998 , Miller 2002 , Strauss 2003 ), Cushing’s syndrome ( Ogo et al. 1991 ), congenital adrenal
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clinical presentation of ACC is frequently characterized by overt Cushing’s syndrome ( Fassnacht et al. 2011 , Else et al. 2014 ). Fertility and the resulting pregnancy rarely occur in Cushing’s syndrome because this condition includes symptoms of