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lüll 11beta-hydroxysteroid dehydrogenase type 1: a tissue-specific regulator of glucocorticoid response Tomlinson JW; Walker EA; Bujalska IJ; Draper N; Lavery GG; Cooper MS; Hewison M; Stewart PMEndocr Rev 2004[Oct]; 25 (5): 831-6611beta-hydroxysteroid dehydrogenase type 1 (11beta-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 11beta-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 "11beta-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 11beta-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 11beta-HSD1 activity. Therapeutic inhibition of 11beta-HSD1 reductase activity in patients with obesity and the metabolic syndrome, as well as in glaucoma and osteoporosis, remains an exciting prospect.|11-beta-Hydroxysteroid Dehydrogenase Type 1/antagonists & inhibitors/chemistry/genetics/*physiology[MESH]|Amino Acid Sequence[MESH]|Animals[MESH]|Carbohydrate Dehydrogenases/genetics[MESH]|Cloning, Molecular[MESH]|Cortisone Reductase/deficiency/genetics[MESH]|Enzyme Inhibitors[MESH]|Gene Expression Regulation, Enzymologic[MESH]|Glaucoma/enzymology[MESH]|Glucocorticoids/*pharmacology[MESH]|Humans[MESH]|Hydrocortisone/metabolism[MESH]|Molecular Sequence Data[MESH]|Mutation[MESH]|NADP/metabolism[MESH]|Obesity/enzymology[MESH]|Organ Specificity[MESH]|Osteoporosis/enzymology[MESH]|Recombinant Proteins[MESH]|Sequence Alignment[MESH]|Substrate Specificity[MESH]|Transcription, Genetic[MESH] |