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• W1592645259 abstract "11Beta-hydroxysteroid dehydrogenases (11beta-HSD) catalyse the interconversion of active glucocorticoids (cortisol, corticosterone) and their inert 11-keto derivatives (cortisone, 11-dehydrocorticosterone). The type-2 isozyme (11beta-HSD-2) is a high-affinity dehydrogenase that catalyses the rapid inactivation of glucocorticoids, thus ensuring selective access of aldosterone to otherwise non-selective mineralocorticoid receptors in the distal nephron. Mutations of the gene encoding 11beta-HSD-2 are responsible for the syndrome of apparent mineralocorticoid excess, in which cortisol illicitly occupies mineralocorticoid receptors, causing hypertension and hypokalaemia. 11Beta-HSD-2 is also highly expressed in the placenta and mid-gestation fetus, where it may protect developing tissues from the often deleterious actions of glucocorticoids upon fetal growth and organ maturation. 11Beta-HSD-1 is probably an 11beta-reductase in vivo. Its function is obscure, but may amplify glucocorticoid action during the diurnal nadir, drawing upon the substantial circulating levels of 11-keto steroids. Both isozymes are regulated during ontogeny and by a series of hormonal and other factors. 11Beta-HSD provide an important control of glucocorticoid action at a cellular level, and may represent new targets for therapeutic intervention." @default.
• W1592645259 created "2016-06-24" @default.
• W1592645259 creator A5064304317 @default.
• W1592645259 creator A5084052287 @default.
• W1592645259 date "1997-10-15" @default.
• W1592645259 modified "2023-10-11" @default.
• W1592645259 title "The 11beta-Hydroxysteroid Dehydrogenase System, A Determinant of Glucocorticoid and Mineralocorticoid Action. Medical and Physiological Aspects of the 11beta-Hydroxysteroid Dehydrogenase System" @default.
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• W1592645259 doi "https://doi.org/10.1111/j.1432-1033.1997.t01-1-00361.x" @default.
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