Corticosteroid 11-beta-dehydrogenase isozyme 2

Corticosteroid 11-β-dehydrogenase isozyme 2 also known as 11-β-hydroxysteroid dehydrogenase 2 is an is_associated_with::enzyme that in humans is encoded by the HSD11B2 is_associated_with::gene.

Function
Corticosteroid 11-β-dehydrogenase isozyme 2 is an NAD+-dependent enzyme expressed in is_associated_with::aldosterone-selective epithelial tissues such as the kidney, colon, salivary and sweat glands. HSD211B2 expression is also found in the is_associated_with::brainstem in a small, aldosterone-sensitive subset of neurons located in the is_associated_with::nucleus of the solitary tract referred to as is_associated_with::HSD2 neurons.

In these tissues, HSD11B2 oxidizes the glucocorticoid is_associated_with::cortisol to the inactive metabolite is_associated_with::cortisone, thus preventing illicit activation of the is_associated_with::mineralocorticoid receptor. This protective mechanism is necessary because cortisol circulates at 100-1000-fold higher concentrations than aldosterone, and binds with equal affinity to the mineralocorticoid receptor, thereby out-competing aldosterone in cells that do not produce HSD11B2.

This glucocorticoid-inactivating enzyme is also expressed in tissues that do not express the mineralocorticoid receptor, such as the placenta and testis, as well as parts of the developing brain, including the rhombencephalic progentitor cells that proliferate into cerebellar is_associated_with::granule cells. In these tissues, HSD11B2 protects cells from the growth-inhibiting and/or pro-apoptotic effects of cortisol, particularly during embryonic development.

Clinical significance
Inhibition of this enzyme, for example by a compound in liquorice, results in a condition known as is_associated_with::pseudohyperaldosteronism. A genetically inherited deficiency of HSD11B2 is the underlying cause of the is_associated_with::syndrome of apparent mineralocorticoid excess.