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
Hipopotasemia asociada al consumo de regaliz
Ana Moreno-Rodrigo,Alfonso Gutiérrez-Macías,Paula Arriola-Martínez,Nicanor García-Jiménez,Esperanza Montero-Aparicio,Felipe Miguel de la Villa +5 more
TL;DR: Las potenciales graves consecuencias y the sencillez de su tratamiento, interrumpiendo el consumo de regaliz y con suplementos de potasio, hacen recomendable that los clinicos estemos familiarizados with this efecto adverso poco habitual of productos alimentarios considerados como seguros.
Dissertation
The role of steroid hormones in skeletal muscle metabolism
TL;DR: Modulation of steroid hormone actions at specific regulatory steps may provide potential therapeutic entry points for metabolic disease and Type 2 diabetes, and attention should be focused on understanding sex-dependent differences in metabolic disease.
Journal ArticleDOI
Especificidad de acción de la aldosterona e hipertensión arterial
TL;DR: La enzima 11 beta-hidroxiesteroide deshidrogenasa tipo 2 (11βHSD2) confiere la especificidad de la accion de the aldosterona respecto a otros corticoides circulantes (cortisol) en los tejidos that deben responder de forma espespecifica a los mineralocorticoides.
Journal ArticleDOI
Increased ACTH Levels Do not Alter Renal 11β- Hydroxysteroid Dehydrogenase Type 2 Gene Expression in the Sheep
TL;DR: It is demonstrated in this study that the expression of 11betaHSD2 in the kidney is unaltered by ACTH, which is likely to be in part due to end product inhibition or substrate overload of the enzyme by endogenous substrates (cortisol, corticosterone, etc) rather than inhibition at the transcriptional level by either ACTH or ACTH regulated steroids.
Book ChapterDOI
Cortisol Metabolism as a Regulator of the Tissue-Specific Glucocorticoid Action
TL;DR: The prereceptor regulation of glucocorticoid action is therefore not only of fundamental physiological and pathological importance, but continues to represent an area of intense scientific and therapeutic interest.
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.
Journal ArticleDOI
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.
Journal ArticleDOI
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.
Journal ArticleDOI
Anti-escherichia coli alpha-haemolysin in control and patient sera
Journal ArticleDOI
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.