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11β-hydroxysteroid Dehydrogenase

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Title: 11β-hydroxysteroid Dehydrogenase  
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Subject: Secondary hypertension, Apparent mineralocorticoid excess syndrome, Carbenoxolone
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11β-hydroxysteroid Dehydrogenase

11-beta-hydroxysteroid dehydrogenase (NADP+)
EC number CAS number IntEnz BRENDA ExPASy KEGG MetaCyc metabolic pathway
PRIAM PDB structures PDBsum
Gene Ontology EGO

11β-Hydroxysteroid dehydrogenase (HSD-11β or 11β-HSD) is the name of a family of enzymes that catalyze the conversion of inert 11 keto-products (cortisone) to active cortisol, or vice versa,[1] thus regulating the access of glucocorticoids to the steroid receptors:

11β-hydroxysteroid + NADP+ \rightleftharpoons an 11-oxosteroid + NADPH + H+

Thus, the two substrates of this enzyme are 11beta-hydroxysteroid and NADP+, whereas its 3 products are 11-oxosteroid, NADPH, and H+.

This enzyme belongs to the family of oxidoreductases, specifically those acting on the CH-OH group of donor with NAD+ or NADP+ as acceptor. The systematic name of this enzyme class is 11beta-hydroxysteroid:NADP+ 11-oxidoreductase. Other names in common use include corticosteroid 11beta-dehydrogenase, beta-hydroxysteroid dehydrogenase, 11beta-hydroxy steroid dehydrogenase, corticosteroid 11-reductase, and dehydrogenase, 11beta-hydroxy steroid. This enzyme participates in c21-steroid hormone metabolism and androgen and estrogen metabolism.

Structural studies

As of late 2007, 8 2IRW.


Cortisol, a glucocorticoid, binds the glucocorticoid receptor. However, because of its molecular similarity to aldosterone it is also capable of binding the mineralcorticoid receptor. Both aldosterone and cortisol have a similar affinity for the mineralocorticoid receptor; however, there is vastly more cortisol in circulation than aldosterone. To prevent over-stimulation of the mineralocorticoid receptor by cortisol, HSD-11β converts the biologically active cortisol to the inactive cortisone, which can no longer bind to the mineralocorticoid receptor. HSD-11β co-localizes with intracellular adrenal steroid receptors. Licorice or Carbenoxolone, which contains glycyrrhetinic acid, can inhibit 11β-HSD and lead to a mineralocorticoid excess syndrome.


In humans, there are two HSD11B isoforms:[2][3]

HSD11B1 NADPH-dependent Highly expressed in key metabolic tissues including liver, adipose tissue, and the central nervous system. In these tissues, HSD11B1 reduces cortisone to the active hormone cortisol that activates glucocorticoid receptors.
HSD11B2 NAD+-dependent Expressed in aldosterone-selective tissues, including kidneys, colon, salivary glands, and placenta. In these tissues, HSD11B2 oxidizes cortisol to cortisone and prevents illicit activation of the mineralocorticoid receptor.

Inhibition of HSD11B1 has been suggested as a possible therapy for treatment of obesity and metabolic syndrome.[3]

See also


External links

  • Medical Subject Headings (MeSH)
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