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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Journal ArticleDOI
Carbenoxolone increases hepatic insulin sensitivity in man: a novel role for 11-oxosteroid reductase in enhancing glucocorticoid receptor activation.
TL;DR: It is inferred that carbenoxolone, by inhibiting hepatic 11 beta-reductase and reducing intrahepatic cortisol concentration, increases hepatic insulin sensitivity and decreases glucose production, and plasma cortisone provides an inactive pool that can be converted to active glucocorticoids at sites where 11 Beta-Reductase is expressed.
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Prenatal glucocorticoid exposure leads to offspring hyperglycaemia in the rat: studies with the 11 b -hydroxysteroid dehydrogenase inhibitor carbenoxolone
TL;DR: The data support the notion that defiency of placental 11 β -HSD, by exposing the fetus to excess maternal glucocorticoids, reduces growth and predisposes to hyperglycaemia in later life.
Journal ArticleDOI
Glucocorticoids, feto-placental 11 beta-hydroxysteroid dehydrogenase type 2, and the early life origins of adult disease.
TL;DR: Feto-placental 11 beta-HSD2, by regulating fetal exposure to maternal glucocorticoids, crucially determines fetal growth and the programming of later disorders.
Journal ArticleDOI
GLUCOCORTICOID AND MINERALOCORTICOID RECEPTORS: Biology and Clinical Relevance
TL;DR: Physiological roles for aldosterone and glucocorticoid membrane receptors, and for the recently described nuclear receptors for 11-ketosteroids in 11 beta-hydroxysteroid dehydro-genase-protected epithelia, remain to be established.
Journal Article
Glucocorticoids, stress, and fertility.
TL;DR: Maternal exposure to prenatal stress or exogenous glucocorticoids can lead to permanent modification of hypothalamo-pituitary-adrenal function and stress-related behaviors in offspring, and the anatomical sites at which these effects take place are reviewed.
References
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Journal ArticleDOI
Mineralocorticoid action: target tissue specificity is enzyme, not receptor, mediated
TL;DR: The presence of the enzyme 11 beta-hydroxy-steroid dehydrogenase, which converts cortisol and corticosterone, but not aldosterone, to their 11-keto analogs, means that these analogs cannot bind to mineralocorticoid receptors.
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LOCALISATION OF 11β-HYDROXYSTEROID DEHYDROGENASE—TISSUE SPECIFIC PROTECTOR OF THE MINERALOCORTICOID RECEPTOR
C. R. W. Edwards,D. Burt,M.A. Mcintyre,E.R. de Kloet,Paul M. Stewart,Lawrence P. Brett,W. Sutanto,Carl Monder +7 more
TL;DR: Findings seem to explain why sodium retention, hypokalaemia, and hypertension develop in subjects with congenital deficiency of 11 beta-OHSD and those in whom the enzyme has been inhibited by liquorice.
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A workbench for multiple alignment construction and analysis.
TL;DR: An interactive program, MACAW (Multiple Alignment Construction and Analysis Workbench), that allows the user to construct multiple alignments by locating, analyzing, editing, and combining “blocks” of aligned sequence segments.
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Anti-escherichia coli alpha-haemolysin in control and patient sera
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Mineralocorticoid activity of liquorice: 11-beta-hydroxysteroid dehydrogenase deficiency comes of age
TL;DR: It is suggested that in both conditions there is a defect in the renal conversion of cortisol to cortisone by 11 beta-OHSD which results in high intrarenal cortisol levels, acting on type 1 mineralocorticoid receptors to cause sodium retention.