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Titolo:
Cortisol metabolism and the role of II beta-hydroxysteroid dehydrogenase
Autore:
Tomlinson, JW; Stewart, PM;
Indirizzi:
Univ Birmingham, Queen Elizabeth Hosp, Div Med Sci, Birmingham B15 2TH, W Midlands, England Univ Birmingham Birmingham W Midlands England B15 2TH W Midlands, England
Titolo Testata:
BEST PRACTICE & RESEARCH CLINICAL ENDOCRINOLOGY & METABOLISM
fascicolo: 1, volume: 15, anno: 2001,
pagine: 61 - 78
SICI:
1521-690X(200103)15:1<61:CMATRO>2.0.ZU;2-1
Fonte:
ISI
Lingua:
ENG
Soggetto:
APPARENT MINERALOCORTICOID EXCESS; TYPE-2 11-BETA-HYDROXYSTEROID DEHYDROGENASE; POLYCYSTIC-OVARY-SYNDROME; RECEPTOR GENE-EXPRESSION; GRANULOSA-LUTEIN CELLS; IN-VITRO FERTILIZATION; ADIPOSE STROMAL CELLS; NECROSIS-FACTOR-ALPHA; GROWTH-HORMONE; SEXUAL DIMORPHISM;
Keywords:
II beta-hydroxysteroid dehydrogenase; apparent mineralocorticoid excess; apparent cortisone reductase deficiency; obesity; hypertension;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
91
Recensione:
Indirizzi per estratti:
Indirizzo: Stewart, PM Univ Birmingham, Queen Elizabeth Hosp, Div Med Sci, BirminghamB15 2TH, W Midlands, England Univ Birmingham Birmingham W Midlands England B15 2TH England
Citazione:
J.W. Tomlinson e P.M. Stewart, "Cortisol metabolism and the role of II beta-hydroxysteroid dehydrogenase", BEST PRAC R, 15(1), 2001, pp. 61-78

Abstract

Two isoforms of the enzyme 11 beta -hydroxysteroid dehydrogenase (11 beta -HSD) interconvert the active glucocorticoid, cortisol, and inactive cortisone. 11 beta -HSDI is believed to act in vivo predominantly as an oxo-reductase using NADP(H) as a cofactor to generate cortisol. In contrast, 11 beta-HSD2 acts exclusively as an MAD-dependent dehydrogenase inactivating cortisol to cortisone, thereby protecting the mineralocorticoid receptor from occupation by cortisol. In peripheral tissues, both enzymes serve to controlthe availability of cortisol to bind to the corticosteroid receptors. Defective expression of 11 beta -HSD2 is implicated in patients with hypertension and intra-uterine growth retardation, while 11 beta -HSDI appears to be intricately involved in the conditions of apparent cortisone reductase deficiency, insulin resistance and visceral obesity. The ability of peripheral tissues to regulate corticosteroid concentrations through 11 beta -HSD isozymes is established as an important mechanism inthe pathogenesis of diverse human diseases. Modulation of enzyme activity may offer a novel therapeutic approach to treating human disease while circumventing the consequences of systemic glucocorticoid excess or deficiency.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 21/07/18 alle ore 00:05:21