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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
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Department of Women’s and Children’s Health, Karolinska Institutet and Pediatric Endocrinology Unit, Karolinska University Hospital, Stockholm, Sweden
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Introduction and background It is estimated that, at any one time, over 250,000 people are exposed to systemic glucocorticoids (GCs); approximately 10% of children will require GCs at some stage during their childhood ( Mushtaq & Ahmed 2002
Department of Internal Medicine, National Taiwan University Hospital, Taiwan
Division of Cancer Research, National Health Research Institutes, No. 7 Chung-Shan South Rd, Taipei 10016, Taiwan
Institute of Toxicology, National Taiwan University College of Medicine, No. 1 Jen Ai Road Section 1, Taipei 100, Taiwan
Department of Internal Medicine, National Taiwan University College of Medicine, Taiwan
Graduate Institute of Clinical Medicine, National Taiwan University College of Medicine, Taiwan
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Department of Internal Medicine, National Taiwan University Hospital, Taiwan
Division of Cancer Research, National Health Research Institutes, No. 7 Chung-Shan South Rd, Taipei 10016, Taiwan
Institute of Toxicology, National Taiwan University College of Medicine, No. 1 Jen Ai Road Section 1, Taipei 100, Taiwan
Department of Internal Medicine, National Taiwan University College of Medicine, Taiwan
Graduate Institute of Clinical Medicine, National Taiwan University College of Medicine, Taiwan
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Department of Internal Medicine, National Taiwan University Hospital, Taiwan
Division of Cancer Research, National Health Research Institutes, No. 7 Chung-Shan South Rd, Taipei 10016, Taiwan
Institute of Toxicology, National Taiwan University College of Medicine, No. 1 Jen Ai Road Section 1, Taipei 100, Taiwan
Department of Internal Medicine, National Taiwan University College of Medicine, Taiwan
Graduate Institute of Clinical Medicine, National Taiwan University College of Medicine, Taiwan
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Department of Internal Medicine, National Taiwan University Hospital, Taiwan
Division of Cancer Research, National Health Research Institutes, No. 7 Chung-Shan South Rd, Taipei 10016, Taiwan
Institute of Toxicology, National Taiwan University College of Medicine, No. 1 Jen Ai Road Section 1, Taipei 100, Taiwan
Department of Internal Medicine, National Taiwan University College of Medicine, Taiwan
Graduate Institute of Clinical Medicine, National Taiwan University College of Medicine, Taiwan
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Department of Internal Medicine, National Taiwan University Hospital, Taiwan
Division of Cancer Research, National Health Research Institutes, No. 7 Chung-Shan South Rd, Taipei 10016, Taiwan
Institute of Toxicology, National Taiwan University College of Medicine, No. 1 Jen Ai Road Section 1, Taipei 100, Taiwan
Department of Internal Medicine, National Taiwan University College of Medicine, Taiwan
Graduate Institute of Clinical Medicine, National Taiwan University College of Medicine, Taiwan
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Department of Internal Medicine, National Taiwan University Hospital, Taiwan
Division of Cancer Research, National Health Research Institutes, No. 7 Chung-Shan South Rd, Taipei 10016, Taiwan
Institute of Toxicology, National Taiwan University College of Medicine, No. 1 Jen Ai Road Section 1, Taipei 100, Taiwan
Department of Internal Medicine, National Taiwan University College of Medicine, Taiwan
Graduate Institute of Clinical Medicine, National Taiwan University College of Medicine, Taiwan
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Introduction Co-administration of glucocorticoids (GCs) with anti-cancer drugs such as cisplatin is a common clinical practice used to prevent drug-induced allergic reaction or nausea/ vomiting ( The Italian Group of Anticancer
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; and local glucocorticoid action, as determined by the abundance of glucocorticoid receptor (GR) and isoforms of 11 β-hydroxysteroid dehydrogenase (11βHSD). The locations and postulated roles of UCP2, VDAC and cytochrome c are outlined in Fig. 1
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Introduction Glucocorticoid (GC) is a significant hormone in regulating diverse physiological processes such as immune and inflammation responses, cell proliferation, differentiation, and apoptosis ( Dondi et al . 2001 , Kudawara et al . 2001
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Glucocorticoids and mineralocorticoids regulate diverse functions important to maintain central nervous system, cardiovascular, metabolic, and immune homeostasis. The actions of these hormones are mediated by their specific intracellular receptors: the glucocorticoid (GR) and mineralocorticoid (MR) receptors. Pathologic conditions associated with changes of tissue sensitivity to these hormones have been described. The syndrome of familial glucocorticoid resistance is characterized by hypercortisolism without Cushing's syndrome stigmata. The molecular defects of four kindreds and one sporadic case have been elucidated as inactivating mutations in the ligand-binding domain of GR. Two cases developed glucocorticoid resistance at the heterozygous state. In these patients, mutant receptors possessed transdominant negative activity upon the wild type receptor. Insensitivity to mineralocorticoids (which may also be caused by loss of function mutations of the MR gene) was found in one sporadic case and four autosomal dominant cases of Pseudohypoaldosteronism type 1. These included two frameshift mutations and a premature termination codon in exon 2, leading to gene products lacking the entire DNA- and ligand-binding domains, and a single base-pair deletion in the intron-5 splice donor site. Tissue hypersensitivity to glucocorticoids was recently hypothesized in patients with Human Immunodeficiency Virus (HIV) type-1 infection via the accessory proteins Vpr and Tat which enhance GR transactivation. Since HIV-1 long terminal repeat (LTR) and glucocorticoid-responsive promoters use the same set of coactivators, these proteins may stimulate HIV-1-LTR and glucocorticoid-inducible genes concurrently. The former may directly stimulate viral proliferation, while the latter may indirectly enhance viral propagation by suppressing the host immune system through glucocorticoid-mediated mechanisms.
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Introduction Glucocorticoids or (gluco)corticosteroids (GCs) are a mainstay in the treatment of chronic inflammatory lung diseases, although their effectiveness is reduced in several diseases. A poor response and a need for higher doses of GCs
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Introduction Glucocorticoids (GCs), such as cortisol in humans and corticosterone in rodents, are produced in the adrenal cortex and play a key role in the regulation of glucose homeostasis and nutrient metabolism. Synthetic GCs, which include
Division of Integrative Physiology, Department of Surgery, Department of Physiology
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Introduction Induction and progression of diabetes under stress conditions involve elevated plasma glucocorticoid levels, owing to activation of the hypothalamic–pituitary–adrenal axis and sympathetic nervous system ( Chan et al . 2002 , Tsigos
Djavad Mowafaghian Centre for Brain Health, University of British Columbia, Vancouver, British Columbia, Canada
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Faculty of Medicine, University of British Columbia, Vancouver, British Columbia, Canada
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Djavad Mowafaghian Centre for Brain Health, University of British Columbia, Vancouver, British Columbia, Canada
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Djavad Mowafaghian Centre for Brain Health, University of British Columbia, Vancouver, British Columbia, Canada
Department of Psychology, University of British Columbia, Vancouver, British Columbia, Canada
Graduate Program in Neuroscience, University of British Columbia, Vancouver, British Columbia, Canada
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, resulting in higher adult baseline and stress-induced glucocorticoid (GC) levels ( Plotsky & Meaney 1993 , Liu et al. 2000 , Lehmann et al. 2002 , O’Mahony et al. 2009 , Lajud et al. 2012 , Vargas et al. 2016 ). The effects of ELS on the
