11β-Hydroxysteroid Dehydrogenase (HSD11B) is the name of a family of enzymes that catalyzes 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.
 Cortisol. Note the OH at the 11 position on ring C. (The other differences between the diagrams are not of consequence.) |
Isoforms
In humans, there are two HSD11B isoforms: [2]
| 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. | In these tissues, HSD11B2 oxidizes cortisol to cortisone and prevents illicit activation of the mineralocorticoid receptor. |
HSD11B2 (11β-hydroxysteroid dehydrogenase type 2) normally inactivates cortisol in the kidney. Cortisol otherwise acts on and activates the same receptor as the hormone aldosterone in the kidney, which in the absence of HSD11B2 would mimic hyperaldosteronism with its effects, like hypokalemia and serious increases in blood pressure, a syndrome known as apparent mineralocorticoid excess.
Large doses of glycyrrhizinic acid and glycyrrhetinic acid in liquorice extract can inhibit this HSD11B2, and thus cause lead to apparent mineralocorticoid excess.
References
- ^ Seckl JR, Walker BR (April 2001). "Minireview: 11beta-hydroxysteroid dehydrogenase type 1- a tissue-specific amplifier of glucocorticoid action". Endocrinology 142 (4): 1371–6. PMID 11250914. http://endo.endojournals.org/cgi/pmidlookup?view=long&pmid=11250914.
- ^ Seckl JR (January 1997). "11beta-Hydroxysteroid dehydrogenase in the brain: a novel regulator of glucocorticoid action?". Front Neuroendocrinol 18 (1): 49–99. doi:. PMID 9000459. http://linkinghub.elsevier.com/retrieve/pii/S0091-3022(96)90143-0.
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