11-beta-hydroxysteroid dehydrogenase

11-β-hydroxysteroid dehydrogenase

two isoenzymes associated with the interconversion of cortisol and cortisone. In the kidney and placenta, reaction is toward cortisone (enzyme type 2) that is inactive as both a glucocorticoid and a mineralocorticoid. This protects the fetus from cortisol-induced salt retention and from the mother's glucocorticoid. Congenital or pharmacologically induced deficiency of this enzyme causes hypertension and electrolyte abnormalities. In liver and adipose tissue, reaction is toward cortisol (enzyme type 1) that is active as both a glucocorticoid and a mineralocorticoid. Knock-out of the gene that codes for this enzyme protects experimental animals from obesity.
References in periodicals archive ?
Global Markets Direct's, 'Corticosteroid 11-Beta-Dehydrogenase Isozyme 1 (11-Beta-Hydroxysteroid Dehydrogenase 1 or Short Chain Dehydrogenase/Reductase Family 26C Member 1 or 11-DH or 11-beta-HSD1 or HSD11B1 or EC 1.1.1.146) - Pipeline Review, H1 2016', provides in depth analysis on Corticosteroid 11-Beta-Dehydrogenase Isozyme 1 (11-Beta-Hydroxysteroid Dehydrogenase 1 or Short Chain Dehydrogenase/Reductase Family 26C Member 1 or 11-DH or 11-beta-HSD1 or HSD11B1 or EC 1.1.1.146) targeted pipeline therapeutics.
The report provides comprehensive information on the Corticosteroid 11-Beta-Dehydrogenase Isozyme 1 (11-Beta-Hydroxysteroid Dehydrogenase 1 or Short Chain Dehydrogenase/Reductase Family 26C Member 1 or 11-DH or 11-beta-HSD1 or HSD11B1 or EC 1.1.1.146), targeted therapeutics, complete with analysis by indications, stage of development, mechanism of action (MoA), route of administration (RoA) and molecule type.
Since glucocorticoids (cortisol in humans and corticosterone in rodents) and mineralocorticoids (aldosterone) both bind to MR with relatively high affinity, the MR specificity of aldosterone in epithelial cells in humans is due to the intracellular inactivation of cortisol to cortisone (and corticosterone to 11-dehydrocorticosterone in rodents) by the enzyme 11-beta-hydroxysteroid dehydrogenase type 2 (11HSD2) (Figure 1).
A well-appreciated but important distinction to make is that a deglycyrrhizinated licorice (DGL) preparation be employed for treatment of GI disorders; glycyrrhizinic acid has the effect of inhibiting the enzyme (11-beta-hydroxysteroid dehydrogenase) responsible for converting cortisol to cortisone.
Cortisol is involved in the distribution and deposition of fat, which is regulated by an enzyme called 11-beta-hydroxysteroid dehydrogenase," Decio Armanini, MD, professor of endocrinology at the University of Padua in Italy, tells Life Extension.
The mechanisms leading to central fat accumulation are more difficult to rationalize, but attention is turning to dysregulation of the enzyme 11-beta-hydroxysteroid dehydrogenase type 1 (11-[beta]-HSD1), which is expressed more in visceral than peripheral fat.