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Iwona J. Bujalska
Researcher at University of Birmingham
Publications - 42
Citations - 5433
Iwona J. Bujalska is an academic researcher from University of Birmingham. The author has contributed to research in topics: Adipose tissue & 11β-hydroxysteroid dehydrogenase type 1. The author has an hindex of 30, co-authored 42 publications receiving 5140 citations. Previous affiliations of Iwona J. Bujalska include University of Giessen.
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Journal ArticleDOI
11beta-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,Paul M. Stewart +7 more
TL;DR: It is speculated 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.
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Does central obesity reflect Cushing's disease of the omentum?
TL;DR: Adipose stromal cells from omental fat, but not subcutaneous fat, can generate active cortisol from inactive cortisone through the expression of 11 beta-HSD1, suggesting that central obesity may reflect "Cushing's disease of the omentum".
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Mutations in the genes encoding 11β-hydroxysteroid dehydrogenase type 1 and hexose-6-phosphate dehydrogenase interact to cause cortisone reductase deficiency
Nicole Draper,Elizabeth A. Walker,Iwona J. Bujalska,Jeremy W. Tomlinson,Susan M Chalder,Wiebke Arlt,Gareth G. Lavery,Oliver Bedendo,David W. Ray,Ian Laing,Ewa M. Malunowicz,Perrin C. White,Martin Hewison,Philip J. Mason,John M. C. Connell,Cedric H.L. Shackleton,Paul M. Stewart +16 more
TL;DR: A defect in the gene HSD11B1 encoding 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1), a primary regulator of tissue-specific glucocorticoid bioavailability, is suggested and H6PDH is established as a potential factor in the pathogenesis of PCOS.
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Differentiation of adipose stromal cells: the roles of glucocorticoids and 11beta-hydroxysteroid dehydrogenase.
TL;DR: Findings indicate that local metabolism of glucocorticoid may control differentiation of adipose tissue in a site-specific fashion and specific inhibitors of 11betaHSD1 may offer a novel approach for the treatment of patients with central obesity.
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Modulation of 11beta-hydroxysteroid dehydrogenase isozymes by proinflammatory cytokines in osteoblasts: an autocrine switch from glucocorticoid inactivation to activation.
Mark S. Cooper,Iwona J. Bujalska,Elizabeth H. Rabbitt,Elizabeth A. Walker,Rosemary Bland,Michael C. Sheppard,Martin Hewison,Paul M. Stewart +7 more
TL;DR: It can be postulated that some of the effects of proinflammatory cytokines within bone (e.g., periarticular erosions in inflammatory arthritis) are mediated by this mechanism.