11ß-Hydroxysteroid Dehydrogenase Type 1: A Tissue-Specific Regulator of Glucocorticoid Response
Jeremy W. Tomlinson,
Elizabeth A. Walker,
Iwona J. Bujalska,
Nicole Draper,
Gareth G. Lavery,
Mark S. Cooper,
Martin Hewison and
Paul M. Stewart
Endocrinology, Division of Medical Sciences, University of Birmingham, Queen Elizabeth Hospital, Edgbaston, Birmingham B15 2TH, United Kingdom
Correspondence: Address all correspondence and requests for reprints to: Paul M. Stewart, M.D., FRCP FMedSci, Professor of Medicine, Division of Medical Sciences, University of Birmingham, Queen Elizabeth Hospital, Edgbaston, B15 2TH, United Kingdom. E-mail: p.m.stewart{at}bham.ac.uk
11ß-Hydroxysteroid dehydrogenase type 1 (11ß-HSD1)interconverts inactive cortisone and active cortisol. Althoughbidirectional, in vivo it is believed to function as a reductasegenerating active glucocorticoid at a prereceptor level, enhancingglucocorticoid receptor activation. In this review, we discussboth the genetic and enzymatic characterization of 11ß-HSD1,as well as describing its role in physiology and pathology ina tissue-specific manner. The molecular basis of cortisone reductasedeficiency, the putative "11ß-HSD1 knockout state"in humans, has been defined and is caused by intronic mutationsin HSD11B1 that decrease gene transcription together with mutationsin hexose-6-phosphate dehydrogenase, an endoluminal enzyme thatprovides reduced nicotinamide-adenine dinucleotide phosphateas cofactor to 11ß-HSD1 to permit reductase activity.We speculate that hexose-6-phosphate dehydrogenase activityand therefore reduced nicotinamide-adenine dinucleotide phosphatesupply may be crucial in determining the directionality of 11ß-HSD1activity. Therapeutic inhibition of 11ß-HSD1 reductaseactivity in patients with obesity and the metabolic syndrome,as well as in glaucoma and osteoporosis, remains an excitingprospect.
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[Abstract][Full Text][PDF]
R. S. Chriguer, L. L. K. Elias, I. M. da Silva Jr., J. G. H. Vieira, A. C. Moreira, and M. de Castro Glucocorticoid Sensitivity in Young Healthy Individuals: in Vitro and in Vivo Studies
J. Clin. Endocrinol. Metab.,
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[Abstract][Full Text][PDF]
P. C. White Genotypes at 11{beta}-Hydroxysteroid Dehydrogenase Type 11B1 and Hexose-6-Phosphate Dehydrogenase Loci Are Not Risk Factors for Apparent Cortisone Reductase Deficiency in a Large Population-Based Sample
J. Clin. Endocrinol. Metab.,
October 1, 2005;
90(10):
5880 - 5883.
[Abstract][Full Text][PDF]
C. van Kooten and A. M. Woltman CD40 brings the shuttle down
Blood,
September 15, 2005;
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L. Freeman, M. Hewison, S. V. Hughes, K. N. Evans, D. Hardie, T. K. Means, and R. Chakraverty Expression of 11{beta}-hydroxysteroid dehydrogenase type 1 permits regulation of glucocorticoid bioavailability by human dendritic cells
Blood,
September 15, 2005;
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2042 - 2049.
[Abstract][Full Text][PDF]
R. S. Weinstein 11{beta}-HSD: Guardian or Gate Crasher?
IBMS BoneKEy,
September 1, 2005;
2(9):
6 - 13.
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J. L. San Millan, J. I. Botella-Carretero, F. Alvarez-Blasco, M. Luque-Ramirez, J. Sancho, P. Moghetti, and H. F. Escobar-Morreale A Study of the Hexose-6-Phosphate Dehydrogenase Gene R453Q and 11{beta}-Hydroxysteroid Dehydrogenase Type 1 Gene 83557insA Polymorphisms in the Polycystic Ovary Syndrome
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F. Hammer, S. Subtil, P. Lux, C. Maser-Gluth, P. M. Stewart, B. Allolio, and W. Arlt No Evidence for Hepatic Conversion of Dehydroepiandrosterone (DHEA) Sulfate to DHEA: In Vivo and in Vitro Studies
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A. K. Agarwal and R. J. Auchus Minireview: Cellular Redox State Regulates Hydroxysteroid Dehydrogenase Activity and Intracellular Hormone Potency
Endocrinology,
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[Abstract][Full Text][PDF]
E. Seeman and G. J. Strewler Clinical and Basic Research Papers - August 2004 Selections
IBMS BoneKEy,
October 1, 2004;
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1 - 3.
[Full Text][PDF]
