11β-Hydroxysteroid Dehydrogenase Type 1: A Tissue-Specific Regulator of Glucocorticoid Response

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ID: 299858
2004
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Abstract
11β-Hydroxysteroid dehydrogenase type 1 (11β-HSD1) interconverts inactive cortisone and active cortisol. Although bidirectional, in vivo it is believed to function as a reductase generating active glucocorticoid at a prereceptor level, enhancing glucocorticoid receptor activation. In this review, we discuss both the genetic and enzymatic characterization of 11β-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 "11β-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 reduced nicotinamide-adenine dinucleotide phosphate as cofactor to 11β-HSD1 to permit reductase activity. We speculate that hexose-6-phosphate dehydrogenase activity and therefore reduced nicotinamide-adenine dinucleotide phosphate supply may be crucial in determining the directionality of 11β-HSD1 activity. Therapeutic inhibition of 11β-HSD1 reductase activity in patients with obesity and the metabolic syndrome, as well as in glaucoma and osteoporosis, remains an exciting prospect.
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openalex_W2016125985 Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Jeremy Tomlinson, Elizabeth A. Walker, Iwona Bujalska, Nicole Draper, Gareth G. Lavery, Mark S. Cooper, Martin Hewison, Paul M. Stewart
Journal endocrine reviews
Year 2004
DOI
10.1210/er.2003-0031
URL
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