11β-Hydroxysteroid dehydrogenases: Key modulators of glucocorticoid action in vivo

Yuri Kotelevtsev, Jonathan R. Seckl, John J. Mullins

Результат исследований: Вклад в журналСтатьярецензирование

15 Цитирования (Scopus)

Аннотация

Intracellular interconversion of active 11-hydroxy glucocorticoids (cortisol, corticosterone) and inert 11 keto products (cortisone, 11- dehydrocorticosterone) by 11 β-hydroxysteroid dehydrogenase (11 β-HSD) enzymes has emerged as a new, potent mechanism of regulation of glucocorticoid action. 11β-hydroxysteroid dehydrogenase type 1 is a widespread, NADP(H)-dependent enzyme that shows bidirectional activity in tissue homogenates and microsomal preparations but functions predominantly as an 11β-reductase (regenerating active glucocorticoids) in intact cells. 11β-hydroxysteroid dehydrogenase type 2 is a much higher-affinity, NAD- dependent, exclusive 11β-dehydrogenase (glucocorticoid inactivating) enzyme that protects mineralocorticoid receptors in distal nephrons from nonselective activation by glucocorticoids in vivo. This review discusses the physiologic functions of 11β-HSDs and their potential diagnostic and therapeutic implications, as revealed by comparison of specific inhibition of 11β-HSD activity by pharmacologic substances and by genetic mutations (spontaneous in humans; targeted in mice).

Язык оригиналаАнглийский
Страницы (с-по)191-198
Число страниц8
ЖурналCurrent Opinion in Endocrinology and Diabetes
Том6
Номер выпуска3
DOI
СостояниеОпубликовано - 1999
Опубликовано для внешнего пользованияДа

Fingerprint

Подробные сведения о темах исследования «11β-Hydroxysteroid dehydrogenases: Key modulators of glucocorticoid action in vivo». Вместе они формируют уникальный семантический отпечаток (fingerprint).

Цитировать