Tissue-specific glucocorticoid excess in the metabolic syndrome:: 11β-HSD1 as a therapeutic target

Systemic glucocorticoid excess is linked to the development of the metabolic syndrome, a group of metabolic disorders including central obesity and insulin resistance. 11 beta-hydroxysteroid dehydrogenase type 1 (11 beta-HSD1) converts the inert cortisone to the active cortisol in target tissues. The increased expression of 11 beta-HSD1 in the adipose tissue of obese subjects suggests that there could be glucocorticoid excess at the tissue level, which is likely to be involved in the development of the metabolic syndrome. 11 beta-HSD1 inhibitors have been under development as a potential therapy for the treatment of the metabolic syndrome. With the current progress, the future prospects of 11 beta-HSD1 inhibitors are encouraging for providing beneficial metabolic effects.