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Department of Experimental Medicine, Sapienza University of Rome, Rome, Lazio, Italy
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Department of Biological and Medical Sciences, Oxford Brookes University, Oxford, Oxfordshire, UK
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Department of Biological and Medical Sciences, Oxford Brookes University, Oxford, Oxfordshire, UK
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-002 metabolises endogenous glucocorticoids, including cortisol and cortisone, to their 5β-reduced metabolites, 5β-dihydrocortisol and 5β-dihydrocortisone, respectively. The 5β-reduced metabolites are then converted, in a non-rate limiting step, to their inactive
Shanghai Key Laboratory for Assisted Reproduction and Reproductive Genetics, Shanghai, People’s Republic of China
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Shanghai Key Laboratory for Assisted Reproduction and Reproductive Genetics, Shanghai, People’s Republic of China
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developed. The human fetal membranes, composed of the amnion and chorion, possess the largest capacity of cortisol regeneration through the reductase action of 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) among fetal tissues ( Murphy 1977 , 1981
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thought to promote the delivery of cortisol to sites of inflammation ( Hammond et al . 1990 , Lin et al . 2009 ). A metalloprotease (LasB), secreted by the pathogen Pseudomonas aeruginosa, may also contribute to the localized release of cortisol from
Circadian Rhythms Group, Chronophysiology Group, School of Medicine, Max Planck Institute for Biophysical Chemistry, Göttingen, Germany
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Circadian Rhythms Group, Chronophysiology Group, School of Medicine, Max Planck Institute for Biophysical Chemistry, Göttingen, Germany
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Circadian Rhythms Group, Chronophysiology Group, School of Medicine, Max Planck Institute for Biophysical Chemistry, Göttingen, Germany
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protocols, the secretion rhythms of cortisol ( el-Hajj Fuleihan et al . 1997 , Wehr et al . 2001 , Aeschbach et al . 2003 , Scheer et al . 2010 ) and melatonin ( Dijk et al . 1999 , Wehr et al . 2001 , Cain et al . 2010 , Gooley et al . 2011
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cortisol, the principal circulating corticosteroid in teleost fishes, plays a crucial role in curbing passive ion loss across the gill epithelium in FW as cortisol has been shown to elicit a dose-dependent increase in transepithelial resistance (TER) across
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Shanghai Key Laboratory for Assisted Reproduction and Reproductive Genetics, Shanghai, People’s Republic of China
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cortisol-regenerating capacity among fetal tissues in late gestation ( Murphy 1981 ). The expression of cortisol-regenerating enzyme 11β-hydroxysteroid dehydrogenase 1 (11β-HSD1) has been found in virtually all cell types in the membranes ( Sun & Myatt 2003
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University of Melbourne and Baker HDI Department of Cardiometabolic Health and Disease, Melbourne, Australia
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(ER) – all of which demonstrate ligand- and cell-selective actions ( Arriza et al. 1987 ). The MR is unique amongst this family in that it binds several classes of steroid hormone – aldosterone, cortisol (corticosterone in rodents) and progesterone
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(DHEA) by P450c17 (steroid 17α-hydroxylase/17,20-lyase), augmented by cytochrome b5. Pregnenolone and 17α-hydroxypregnenolone are also metabolized to aldosterone and cortisol respectively, via successive reactions of 3β-hydroxysteroid dehydrogenase/Δ 5
Division of Endocrinology, Department of Medicine, Faculté de médecine et des sciences de la santé, Université de Sherbrooke, Sherbrooke, Quebec, Canada
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for 20% of FGD ( Meimaridou et al. 2013 , Jackson et al . 2015 ). FGD is an autosomal recessive disorder resulting in cortisol deficiency, due to resistance of the adrenal cortex to the action of ACTH. Postmortem examination of adrenal glands from
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ABSTRACT
Cells isolated from the zona fasciculata/reticularis (ZFR) of the bovine adrenal cortex and maintained in culture were found to secrete cortisol in response to vasopressin stimulation. The increased cortisol secretion was dose dependent, with a threshold response at 1 nm and a maximal response (1·68-fold over basal) at 0·1 μm. In cells cultured in the presence of [3H]inositol (to prelabel the membrane phosphoinositide pool), stimulation with vasopressin in the presence of LiCl (10 mm) resulted in a similar dose-dependent increase in labelling of the phosphoinositol fraction, with a maximal response (1·45-fold over basal) at 10 nm. The increased labelling of the phosphoinositol fraction was independent of extracellular Ca2+ as it was not abolished in medium with [Ca2+ ] buffered to intracellular resting levels. This suggests that vasopressin stimulation results in the activation of a phosphoinositidase C. It is probable that cortisol secretion by bovine ZFR cells in response to vasopressin is dependent upon activation of this Ca2+-independent phosphoinositidase C. However, the small magnitude of the cortisol secretory response makes it unlikely that vasopressin is a primary regulator of cortisol secretion in vivo.
