Corticosteroid 11-beta-dehydrogenase isozyme 2

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Hydroxysteroid (11-beta) dehydrogenase 2
Symbols HSD11B2 ; AME; AME1; HSD11K; HSD2; SDR9C3
External IDs OMIM614232 MGI104720 HomoloGene20088 ChEMBL: 3746 GeneCards: HSD11B2 Gene
EC number
RNA expression pattern
PBB GE HSD11B2 204130 at tn.png
More reference expression data
Species Human Mouse
Entrez 3291 15484
Ensembl ENSG00000176387 ENSMUSG00000031891
UniProt P80365 P51661
RefSeq (mRNA) NM_000196 NM_008289
RefSeq (protein) NP_000187 NP_032315
Location (UCSC) Chr 16:
67.46 – 67.47 Mb
Chr 8:
105.52 – 105.52 Mb
PubMed search [1] [2]

Corticosteroid 11-β-dehydrogenase isozyme 2 also known as 11-β-hydroxysteroid dehydrogenase 2 is an enzyme that in humans is encoded by the HSD11B2 gene.[1][2][3]


Corticosteroid 11-β-dehydrogenase isozyme 2 is an NAD+-dependent enzyme expressed in aldosterone-selective epithelial tissues such as the kidney, colon, salivary and sweat glands. HSD211B2 expression is also found in the brainstem in a small, aldosterone-sensitive subset of neurons located in the nucleus of the solitary tract referred to as HSD2 neurons.[4]

In these tissues, HSD11B2 oxidizes the glucocorticoid cortisol to the inactive metabolite cortisone, thus preventing illicit activation of the 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 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[edit]

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


  1. ^ Albiston AL, Obeyesekere VR, Smith RE, Krozowski ZS (November 1994). "Cloning and tissue distribution of the human 11 beta-hydroxysteroid dehydrogenase type 2 enzyme". Mol. Cell. Endocrinol. 105 (2): R11–7. doi:10.1016/0303-7207(94)90176-7. PMID 7859916. 
  2. ^ Brown RW, Chapman KE, Kotelevtsev Y, Yau JL, Lindsay RS, Brett L, Leckie C, Murad P, Lyons V, Mullins JJ, Edwards CR, Seckl JR (February 1996). "Cloning and production of antisera to human placental 11 beta-hydroxysteroid dehydrogenase type 2". Biochem. J. 313 ( Pt 3) (Pt 3): 1007–17. PMC 1216963. PMID 8611140. 
  3. ^ "Entrez Gene: HSD11B2 hydroxysteroid (11-beta) dehydrogenase 2". 
  4. ^ Geerling, Joel C.; Arthur D. Loewy (September 2009). "Aldosterone in the brain". American Journal of Physiology, Renal Physiology 297 (3): F559–76. doi:10.1152/ajprenal.90399.2008. PMC 2739715. PMID 19261742. 

Further reading[edit]