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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
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Centre for Systems Health and Integrated Metabolic Research, Department of Biosciences, School of Science and Technology, Nottingham Trent University, Nottingham, UK
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) ( Bravenboer et al. 2020 , Cawthorn 2020 ). Bone marrow adipocytes further accumulate in diverse conditions, including ageing, obesity, type 2 diabetes, osteoporosis, chronic kidney disease, and in iatrogenic contexts such as chronic glucocorticoid treatment
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reporting that Mif - knockout mice display improved insulin sensitivity and glucose tolerance ( Verschuren et al. 2009 , Kleemann & Bucala 2010 ). Although MIF synthesis and secretion are upregulated by the glucocorticoid hormones (GCs), MIF acts as
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
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Introduction The catabolic effects of glucocorticoids have been well known for many years. Either as drugs used to treat several medical conditions or as endocrine hormones released in response to many stress situations, glucocorticoids may cause
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hypothalamus ( Fig. 2 ; Buijs & Kalsbeek 2001 , Kalsbeek & Buijs 2002 , Saper et al . 2005 ), and may underlie the circadian changes observed in processes governed by these structures. Figure 2 Neural pathways in circadian control of glucocorticoid release
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Introduction Glucocorticoids are a class of corticosteroids and are chiefly produced in the zona fasciculata of the adrenal cortex. These steroid hormones are crucial endocrine regulators of body functions in homeostasis and adaptation to
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Introduction Glucocorticoids exert effects on virtually all tissues, the majority of which are mediated by the type II glucocorticoid receptor (GR). Despite near ubiquitous expression, GR levels vary widely both between and within
Cell Biology and Immunology Group, Wageningen University, Marijkeweg 40, 6709 PG, Wageningen, The Netherlands
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Cell Biology and Immunology Group, Wageningen University, Marijkeweg 40, 6709 PG, Wageningen, The Netherlands
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Cell Biology and Immunology Group, Wageningen University, Marijkeweg 40, 6709 PG, Wageningen, The Netherlands
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Cell Biology and Immunology Group, Wageningen University, Marijkeweg 40, 6709 PG, Wageningen, The Netherlands
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Introduction Glucocorticoids (GCs; cortisol and corticosterone) play a pivotal role in vertebrate physiology through a plethora of control mechanisms. The GC system, with a nuclear glucocorticoid receptor (GR), is found in all
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aldosterone, which is bound primarily by albumin, other steroid hormones bind to CBG and SHBG with high (nM) affinity and specificity, with SHBG binding the major androgens and estrogens, and CBG binding the glucocorticoids and progesterone, preferentially