11 beta-Hydroxysteroid dehydrogenase

Vitam Horm. 1999;57:249-324.


In mammalian tissues, at least two isozymes of 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD) catalyze the interconversion of hormonally active C11-hydroxylated corticosteroids (cortisol, corticosterone) and their inactive C11-keto metabolites (cortisone, 11-dehydrocorticosterone). The type 1 and type 2 11 beta-HSD isozymes share only 14% homology and are separate gene products with different physiological roles, regulation, and tissue distribution. 11 beta-HSD2 is a high affinity NAD-dependent dehydrogenase that protects the mineralocorticoid receptor from glucocorticoid excess; mutations in the HSD11B2 gene explain an inherited form of hypertension, the syndrome of apparent mineralocorticoid excess in which cortisol acts as a potent mineralocorticoid. By contrast, 11 beta-HSD1 acts predominantly as a reductase in vivo, facilitating glucocorticoid hormone action in key target tissues such as liver and adipose tissue. Over the 10 years, 11 beta-HSD has progressed from an enzyme merely involved in the peripheral metabolism of cortisol to a crucial pre-receptor signaling pathway in the analysis of corticosteroid hormone action. This review details the enzymology, molecular biology, distribution, regulation, and function of the 11 beta-HSD isozymes and highlights the clinical consequences of altered enzyme expression.

Publication types

  • Review

MeSH terms

  • 11-beta-Hydroxysteroid Dehydrogenases
  • Adrenal Cortex Hormones / metabolism
  • Adrenal Cortex Hormones / physiology
  • Animals
  • Gene Expression Regulation
  • Humans
  • Hydroxysteroid Dehydrogenases* / genetics
  • Hydroxysteroid Dehydrogenases* / physiology
  • Isoenzymes / genetics
  • Mutation
  • Receptors, Steroid / physiology
  • Tissue Distribution


  • Adrenal Cortex Hormones
  • Isoenzymes
  • Receptors, Steroid
  • Hydroxysteroid Dehydrogenases
  • 11-beta-Hydroxysteroid Dehydrogenases