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Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
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Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
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Introduction In patients with malignant disease, glucocorticoids are widely used on various indications. High-dose treatment is given as part of chemotherapy regimens and for treating oedema associated with metastatic spinal cord compression
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DES induced an intrauterine growth restriction of pups in the placentas ( 6 ). However, the mechanism has not been fully elucidated. Figure 1 Chemical structure of cortisol and diethylstilbestrol. Glucocorticoid hormone is an inducing
Department of Pediatrics, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam Reproduction & Development Research Institute, de Boelelaan, Amsterdam, The Netherlands
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Department of Pediatrics, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam Reproduction & Development Research Institute, de Boelelaan, Amsterdam, The Netherlands
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Department of Pediatrics, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam Reproduction & Development Research Institute, de Boelelaan, Amsterdam, The Netherlands
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arterial hypotension ( 13 ). We aimed to examine whether male and female preterm infants differ in cortisol production and metabolism as assessed by glucocorticoid metabolite excretion in urine, as a possible explanation for the sex differences in
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Department of Neurology, Beth Israel Deaconess Medical Center, Boston, Massachusetts, USA
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Department of Medicine, Brigham and Women’s Hospital, Boston, Massachusetts, USA
Harvard Medical School, Boston, Massachusetts, USA
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). Glucocorticoids also have a negative impact on the Wnt/β-catenin pathway leading to an imbalance in bone formation and bone resorption, and thereby contributing to glucocorticoid-induced osteoporosis ( 1 , 3 , 10 , 11 , 12 , 13 ). In mice, glucocorticoids
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, 9 , 10 , 11 , 12 ). Recently, we have demonstrated that the bovine oocyte cumulus complex (COC) undergoing IVM expresses two types of glucocorticoid metabolizing enzymes, namely 11β-hydroxysteroid oxidoreductase type1 (HSD11B1) and type2 (HSD11B
Department of Endocrinology, The Newcastle upon Tyne Hospitals NHS Foundation Trust, Newcastle upon Tyne, UK
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Department of Endocrinology, The Newcastle upon Tyne Hospitals NHS Foundation Trust, Newcastle upon Tyne, UK
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insufficient to meet the body’s needs. Overt mineralocorticoid deficiency causes the characteristic presentation of salt craving, postural hypotension, hyponatraemia and hyperkalaemia. Glucocorticoid deficiency causes loss of appetite, early satiety, weight
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neural POMC is multifactorial (e.g. (65, 67) , and this is primarily linked to its role in energy balance and nutrition, see text. There is, however, much evidence to show the feedback of glucocorticoids on CRH expression in several brain regions. Mostly
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pathway of the stress response ( 1 ). This in turn, has many peripheral effects, such as an increase in circulating glucocorticoids (GCs) ( 2 , 3 ). Chronic stress or prolonged exogenous GC treatment also disrupts the central homeostatic nature of GC
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Institute of Genetic Medicine, Newcastle University, Newcastle upon Tyne, UK
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). Interaction between gonadal steroids and the metabolism of cortisol has been suggested by several studies ( 21 , 22 , 23 , 24 ). However, there is only one cross-sectional study that has investigated glucocorticoid metabolism in children of various ages
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Department of Physiology, Faculty of Science, Charles University, Prague, Czech Republic
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Department of Physiology, Faculty of Science, Charles University, Prague, Czech Republic
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the sympathetic–adrenal–medullary axis, which subsequently release glucocorticoids and catecholamines, respectively. The HPA and SNS axes are the two major pathways through which stress is able to modulate immune functions depending on the nature