The cortisol-activating enzyme 11β-hydroxysteroid dehydrogenase type 1 in skeletal muscle in the pathogenesis of the metabolic syndrome

Abstract

The enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) contributes to intracellular glucocorticoid action by converting inactive cortisone to its receptor-active form cortisol (11-dehydrocorticosterone and corticosterone in mice and rats). The potential role of 11β-HSD1 in the pathogenesis of the metabolic syndrome has emerged over the past three decades. However, the precise impact of 11β-HSD1 in obesity-related diseases remains uncertain. Many studies from animal experiments to clinical studies have investigated liver and adipose tissue 11β-HSD1 in relation to obesity and its metabolic disorders including insulin resistance. But the relevance of 11β-HSD1 in skeletal muscle has been less extensively studied. On the other hand, skeletal muscle is assumed to be the main site of peripheral insulin resistance, but the biological relevance of 11β-HSD1 in skeletal muscle is unclear. This mini-review will focus on 11β-HSD1 in skeletal muscle and its postulated link to obesity and insulin-resistance.

Keywords: 11β-HSD1; Glucocorticoids; Metabolic syndrome; Obesity; Skeletal muscle.