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• W2022148815 abstract "Increases in plasma cortisol and glucocorticoid pharmacotherapy cause myriad adverse effects from obesity and diabetes to impairments in memory. The common metabolic syndrome phenotypically resembles the rare disorder Cushing's syndrome, but plasma cortisol levels are usually normal. 11β-Hydroxysteroid dehydrogenase type 1 (11β-HSD1) catalyses the regeneration of active glucocorticoids (cortisol and corticosterone) from inert 11-keto forms in specific tissues, notably liver, adipose and brain. Recent work shows that obese humans and rodents have increased 11β-HSD1 activity selectively in adipose tissue. By locally amplifying glucocorticoid action, this increase in activity might explain the Cushing's syndrome/metabolic syndrome paradox. Indeed, mice deficient in 11β-HSD1 resist both the metabolic syndrome that develops with dietary obesity and glucocorticoid-associated cognitive impairments that develop with ageing. The ongoing development of selective 11β-HSD1 inhibitors affords the opportunity to explore a new approach to some major common disorders. Increases in plasma cortisol and glucocorticoid pharmacotherapy cause myriad adverse effects from obesity and diabetes to impairments in memory. The common metabolic syndrome phenotypically resembles the rare disorder Cushing's syndrome, but plasma cortisol levels are usually normal. 11β-Hydroxysteroid dehydrogenase type 1 (11β-HSD1) catalyses the regeneration of active glucocorticoids (cortisol and corticosterone) from inert 11-keto forms in specific tissues, notably liver, adipose and brain. Recent work shows that obese humans and rodents have increased 11β-HSD1 activity selectively in adipose tissue. By locally amplifying glucocorticoid action, this increase in activity might explain the Cushing's syndrome/metabolic syndrome paradox. Indeed, mice deficient in 11β-HSD1 resist both the metabolic syndrome that develops with dietary obesity and glucocorticoid-associated cognitive impairments that develop with ageing. The ongoing development of selective 11β-HSD1 inhibitors affords the opportunity to explore a new approach to some major common disorders." @default.
• W2022148815 created "2016-06-24" @default.
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• W2022148815 date "2004-11-01" @default.
• W2022148815 modified "2023-10-02" @default.
• W2022148815 title "11β-hydroxysteroid dehydrogenase type 1 as a modulator of glucocorticoid action: from metabolism to memory" @default.
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• W2022148815 doi "https://doi.org/10.1016/j.tem.2004.09.007" @default.
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