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HPA axis in depression ( Dinan 1994 ) and chronic fatigue syndrome ( Demitrack et al . 1991 ) could be due to alterations in the mechanisms through which glucocorticoids, secreted by the adrenal cortex, exert inhibitory negative feedback effects on
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Departments of Rheumatology and Inflammation Research, Internal Medicine and Clinical Nutrition, Laboratory of Tumor Immunology and Biology, Centre for Bone and Arthritis Research, Institute of Medicine, The Sahlgrenska Academy, University of Gothenburg, Box 480, Gothenburg 405 30, Sweden
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Departments of Rheumatology and Inflammation Research, Internal Medicine and Clinical Nutrition, Laboratory of Tumor Immunology and Biology, Centre for Bone and Arthritis Research, Institute of Medicine, The Sahlgrenska Academy, University of Gothenburg, Box 480, Gothenburg 405 30, Sweden
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Introduction Glucocorticoids are frequently used for the treatment of noninfectious and autoimmune inflammation as, amongst other mechanisms, they can suppress lymphocytes ( Chantler et al . 2003 , Busillo & Cidlowski 2013 ). Prolonged use of
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identification of potential therapies ( Crane et al. 2015 , Yao et al. 2015 , Maksimov et al. 2016 ). Obesity is related, either as a cause or as a consequence, to the disruption of several hormonal systems. Higher levels of glucocorticoids (GCs) and
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influences, which can modulate fetal development and lead to permanent alterations in the cardiovascular system: these are under nutrition and overexposure to glucocorticoids ( Seckl & Meaney 2004 ). Evidence that overexposure of the fetus to
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Glucocorticoids are widely used to treat inflammatory and malignant diseases. However, many individuals show a lack of therapeutic response and unwanted side-effects. Various known and unknown parameters determine glucocorticoid responsiveness, among them glucocorticoid receptor (GR)-interacting proteins. Several of the proteins interacting with GR also participate in other signal transduction pathways such as the AP-1 pathway and the nuclear factor-kappaB pathway. We suggest that a closer study of GR-interacting proteins may shed new light on mechanisms determining glucocorticoid sensitivity. In this commentary, the general mechanisms of GR action will be addressed and a proteomic-based method to study GR-interacting proteins will be described in brief.
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The Ritchie Centre, Hudson Institute of Medical Research, Clayton, Australia
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Institute for Women’s Health, University College London, London, UK
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Department of Biological and Medical Sciences, Oxford Brookes University, Oxford, UK
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Introduction In adults, glucocorticoids are stress hormones with metabolic actions on a wide range of tissues that maintain functions critical to survival in adverse environmental conditions and during normal physiological challenges to
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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Introduction Glucocorticoid (GC) stress hormones are essential for physiology and exert numerous functions via binding to the glucocorticoid receptor (GR). The predominant active GC hormone is cortisol in humans, while rats and mice adrenals
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glucocorticoid regulated kinase-1 (SGK1). This short commentary looks at SGK1 pathophysiology and discusses the consequences of disturbed SGK1-mediated Na + reabsorption in diabetes in relation to the development of diabetic nephropathy. SGK1 The serum and
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programming of postnatal metabolism has been demonstrated in a number of species using a range of different techniques to induce intrauterine growth restriction (IUGR) including maternal stress and glucocorticoid administration (see McMillen & Robinson 2005
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pronounced hepatomegaly ( Repa et al . 2000 , Honda et al . 2001 , Dubrac et al . 2005 ). The intracellular concentrations of glucocorticoids are modulated by the 11β-hydroxysteroid dehydrogenase (HSD11B) enzyme. HSD11B type 1 (HSD11B1) preferentially