Journal ArticleDOI
Cloning and tissue distribution of the human 1 lβ-hydroxysteroid dehydrogenase type 2 enzyme
TLDR
The 11β-hydroxysteroid dehydrogenase (11βHSD) as mentioned in this paper was found to protect the nonselective mineralocorticoid receptor from occupation by glucocorticity, and to modulate access of glucoc Corticoid to glucoc corticoid receptors resulting in protection of the fetus and gonads.About:
This article is published in Molecular and Cellular Endocrinology.The article was published on 1994-11-01. It has received 678 citations till now. The article focuses on the topics: Glucocorticoid receptor & Apparent mineralocorticoid excess syndrome.read more
Citations
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The molecular biology, biochemistry, and physiology of human steroidogenesis and its disorders.
TL;DR: Understanding steroidogenesis is of fundamental importance to understanding disorders of sexual differentiation, reproduction, fertility, hypertension, obesity, and physiological homeostasis.
Journal ArticleDOI
11beta-hydroxysteroid dehydrogenase type 1: a tissue-specific regulator of glucocorticoid response.
Jeremy W. Tomlinson,Elizabeth A. Walker,Iwona J. Bujalska,Nicole Draper,Gareth G. Lavery,Mark S. Cooper,Martin Hewison,Paul M. Stewart +7 more
TL;DR: It is speculated that hexose-6-phosphate dehydrogenase activity and therefore reduced nicotinamide-adenine dinucleotide phosphate supply may be crucial in determining the directionality of 11beta-HSD1 activity.
Journal ArticleDOI
Molecular Determinants of Glucocorticoid Receptor Function and Tissue Sensitivity to Glucocorticoids
TL;DR: This review has summarized the multiple endogenous and exogenous factors that have been shown to be involved in this signaling cascade and, thus, to alter glucocorticoid sensitivity.
Journal ArticleDOI
Prenatal Stress, Glucocorticoids and the Programming of the Brain
Leonie Welberg,Jonathan R. Seckl +1 more
TL;DR: The data suggest that key targets for programming include glucocorticoid receptor gene expression and the corticotrophin‐releasing hormone system, and that approaches to minimize or reverse the consequences of such early life events may have therapeutic importance.
Journal ArticleDOI
11beta-hydroxysteroid dehydrogenase type 1 knockout mice show attenuated glucocorticoid-inducible responses and resist hyperglycemia on obesity or stress.
Yuri Kotelevtsev,Megan C. Holmes,Ann Burchell,Pamela Houston,Dieter Schmoll,Pauline Jamieson,Ruth Best,Roger W. Brown,Christopher R. W. Edwards,Jonathan R. Seckl,John J. Mullins +10 more
TL;DR: Attenuation of hepatic 11beta-HSD-1 may provide a novel approach to the regulation of gluconeogenesis, which involves regenerating active glucocorticoids from circulating inert 11-keto forms in specific tissues, notably the liver.
References
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Journal ArticleDOI
Dysfunction of placental glucocorticoid barrier: link between fetal environment and adult hypertension?
TL;DR: The lifetime risk of common disorders may be partly determined by the intrauterine environment, supported by findings that in rats decreased activity of the enzyme that acts as a placental barrier to maternal glucocorticoids is associated with low birthweight.
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The neuronal mineralocorticoid eeceptor as a mediator of glucocorticoid response
TL;DR: In vitro assay for MR and GR function demonstrates that these receptors respond to different levels of glucocorticoid, suggesting that together they confer a larger dynamic range of sensitivity to this hormone, leading to a new hypothesis for glucoc Corticosteroid action in the central nervous system.
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Male pseudohermaphroditism caused by mutations of testicular 17β-hydroxysteroid dehydrogenase 3
Wayne M. Geissler,Daphne L. Davis,Ling Wu,Karen D. Bradshaw,S. Patel,Berenice B. Mendonca,Keith O. Elliston,Jean D. Wilson,David W. Russell,Stefan Andersson +9 more
TL;DR: Four substitution and two splice junction mutations were identified in the 17βHSD3 genes of five unrelated male pseudohermaphrodites that severely compromised the activity of the 17 β–HSD type 3 isozyme.
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A Syndrome of Apparent Mineralocorticoid Excess Associated with Defects in the Peripheral Metabolism of Cortisol
Stanley Ulick,L S Levine,Peter Gunczler,G Zanconato,Leyla C. Ramirez,W Rauh,Ariel Rösler,H L Bradlow,Maria I. New +8 more
TL;DR: The decrease in the MCR permitted the maintenance of normal cortisol plasma levels and normal glucocorticoid function at a diminished rate of secretion, and serves as a biochemical marker of this hypertensive syndrome.
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Cloning and expression of rat cDNA encoding corticosteroid 11 beta-dehydrogenase.
TL;DR: A search of sequence databases revealed that 11-DH is identical in about 27% of amino acid residues to ribitol dehydrogenase from Klebsiella and to the product of the nodG gene from the nitrogen-fixing bacterium, Rhizobium meliloti, thus defining a new superfamily of genes encoding dehydrogenases.