Abstract
The enzyme IIβHSD catalyzes the interconversion of the biologically active cortisol and the biologically inactive cortisone. - There are two distinct isozymes: IIβHSD type I is mainly expressed in liver and is a bidirectional enzyme, with both dehydrogenase and reductase activity. IIβHSD type 2 is mainly expressed in kidney and is a unidirectional enzyme with only dehydrogenase activity. - IIβHSD type 2 protects the mineralocorticoid receptor from being activated by cortisol. Thus, specificity of this receptor in vivo is enzyme and not receptor mediated. - The syndrome of apparent mineralocorticoid excess is caused by a congenital deficiency of IIβHSD type 2. - Liquorice-induced hypertension is an example of an acquired defect in dehydrogenase activity of IIβHSD, caused by glycyrrhetinic acid. - IIβHSD may play a role in the pathogenesis of 'essential' hypertension, obesity and type I diabetes mellitus. Angiotensine-converting enzyme inhibitors enhance dehydrogenase activity of IIβHSD, which may contribute to their natriuretic effect.
| Translated title of the contribution | IIβ-hydroxysteroid-dehydrogenase (IIβHSD): Characteristics and clinical impact of a key enzyme in cortisol metabolism |
|---|---|
| Original language | Dutch |
| Pages (from-to) | 509-514 |
| Number of pages | 6 |
| Journal | Nederlands Tijdschrift voor Geneeskunde |
| Volume | 143 |
| Issue number | 10 |
| Publication status | Published - 6-Mar-1999 |