Endocrine Abstracts

Cushing’s disease presents with multiple symptoms of systemic glucocorticoid (GC) excess including increased skin thinning and poor wound healing (WH). Local GC concentrations are regulated by 11β-hydroxysteroid dehydrogenase (11β-HSD) isozymes converting inactive cortisone/11-dehydrocorticosterone to cortisol/corticosterone (11β-HSD1) or vice versa (11β-HSD2). We previously demonstrated elevated 11β-HSD1 activity during early WH, hypothe...

UVB exposure induces skin damage including dermal atrophy, telangiectasia, fragility and poor wound healing; symptoms also attributable to glucocorticoid (GC) excess (e.g. Cushing’s syndrome). In peripheral tissues including skin, GC availability is regulated by 11β-hydroxysteroid dehydrogenase (11β-HSD) types 1/2 which respectively activate/deactivate cortisol (and rodent corticosterone) from/to cortisone (and rodent 11-dehydrocorticosterone). Although we previ...

Glucocorticoid (GC) excess inhibits wound healing (WH) causing increased patient discomfort and infection risk. The GC-activating enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) regulates local GC availability in tissues including liver, adipose, and muscle. 11β-HSD1 is also expressed in skin, where studies recently demonstrated increased levels in older donors and a reversal of age-induced dermal atrophy in 11β-HSD1-null mice. However, the role o...