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 ?
Mineralocorticoid activity of liquorice: 11-beta-hydroxysteroid dehydrogenase deficiency comes of age.
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.
Glycyr-rhetinic acid, the active principal of licorice root, blocks 11-beta-hydroxysteroid dehydrogenase type 1, thus reducing the availability of cortisol at the level of adipocytes.