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-hydroxysteroid dehydrogenase type 1: A tissue-specific regulator of glucocorticoid response
Endocrinology, Division of Medical Sciences, University of Birmingham, Queen Elizabeth Hospital, Edgbaston, Birmingham B15 2TH, UK
* To whom correspondence should be addressed. E-mail: p.m.stewart{at}bham.ac.uk..
11
-hydroxysteroid dehydrogenase type 1 interconverts inactive cortisone and active cortisol. Although bi-directional, in vivo it is believed to function as a reductase generating active glucocorticoid at a pre-receptor level, enhancing glucocorticoid receptor activation. In this review we discuss both the genetic and enzymatic characterization of 11-HSD1 as well as describing its role in physiology and pathology in a tissue specific manner. The molecular basis of Cortisone Reductase Deficiency, the putative '11-HSD1 knockout state' in humans, has been defined and is caused by intronic mutations in HSD11B1 that decrease gene transcription together with mutations in hexose-6-phosphate dehydrogenase, an endoluminal enzyme that provides NADPH as cofactor to 11-HSD1 to permit reductase activity. We speculate that H6PDH activity and therefore NADPH supply may be crucial in determining the directionality of 11-HSD1 activity. Therapeutic inhibition of 11-HSD1 reductase activity in patients with obesity and the metabolic syndrome as well as in glaucoma and osteoporosis remains an exciting prospect.
-hydroxysteroid dehydrogenase type 1 •
cortisol
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