Evidence for transcript-specific epigenetic regulation of glucocorticoid-stimulated skeletal muscle 11β-hydroxysteroid dehydrogenase-1 activity in type 2 diabetes.

Background: The enzyme 11β-hydroxysteroid dehydrogenase type 1 (11βHSD1) converts inactive cortisone into active cortisol in insulin target tissues. In people with type 2 diabetes, skeletal muscle (SkM) 11βHSD1 is upregulated by the potent glucocorticoid dexamethasone. The HSD11B1 gene has two promoters designated P1 and P2.

Dexamethasone administration inhibits skeletal muscle expression of the androgen receptor and IGF-1--implications for steroid-induced myopathy.

Context: Glucocorticoids are a well-recognized cause of muscle weakness. The early effects of glucocorticoids on skeletal muscle (SkM) androgen and IGF-1 pathways have not been previously investigated in human subjects.

Objective: To determine if administration of the potent glucocorticoid dexamethasone down-regulates SkM androgen receptor and the IGF-1 signalling pathway.

Skeletal muscle 11beta hydroxysteroid dehydrogenase type 1 activity is upregulated following elective abdominal surgery.

Objective: Cortisol has been traditionally implicated in the causation of peri-operative skeletal muscle (SkM) insulin resistance, but cortisol levels return to normal within 72 h of surgery. Tissue cortisol bioactivity may be prolonged by local upregulation of the enzyme 11betaHSD1. We aimed to investigate the changes of SkM 11betaHSD1 enzyme activity and mRNA expression, relative to plasma cortisol, insulin and glucose levels following elective abdominal surgery.

Adiponectin, skeletal muscle adiponectin receptor expression and insulin resistance following dexamethasone.

Objective: Skeletal muscle is a major site of adiponectin action and of glucocorticoid-induced insulin resistance. Little human data exist however, regarding the impact of exogenous glucocorticoids on adiponectin receptors in skeletal muscle.

Design And Patients: Twelve subjects with type 2 diabetes and 12 controls underwent blood sampling and muscle biopsy of vastus lateralis before and after 4 days of 4 mg dexamethasone.

Altered activity of 11beta-hydroxysteroid dehydrogenase types 1 and 2 in skeletal muscle confers metabolic protection in subjects with type 2 diabetes.

Context: There is little information regarding the regulation of 11beta-hydroxysteroid dehydrogenase (11beta-HSD) enzymes in skeletal muscle in the setting of type 2 diabetes.

Objective: Our objective was to investigate whether there is differential mRNA expression and enzyme activity of 11beta-HSD1 and 11beta-HSD2 in the skeletal muscle of diabetic subjects compared with controls at baseline and in response to dexamethasone.

Design: Participants underwent muscle biopsy of vastus lateralis at baseline and after dexamethasone.

11Beta hydroxysteroid dehydrogenase type 1 is expressed and is biologically active in human skeletal muscle.

Objective: No data exist regarding the distribution and oxoreductase enzyme activity of 11beta hydroxysteroid dehydrogenase type 1 (11beta HSD-1) in fresh human skeletal muscle. We aimed to investigate the mRNA and protein expression of 11beta HSD-1 in fresh skeletal muscle, confirm its biological activity and determine its relationship with hexose-6-phosphate dehydrogenase (H6PDH). We also examined the muscle fibre localization of 11beta HSD-1.

Aromatase-deficient (ArKO) mice have reduced blood pressure and baroreflex sensitivity.

Aromatase-deficient (ArKO) mice are deficient in estrogens due to deletion of the aromatase gene. We hypothesized that there may be changes in the cardiovascular system of ArKO mice because of evidence linking estrogens with improved cardiovascular outcomes and the induction of the glucocorticoid-metabolizing enzyme, 11beta-hydroxysteroid dehydrogenase type 2 (11betaHSD2), gene in the kidney, which is important for the regulation of blood pressure (BP). BP and baroreflex sensitivity (BRS) in female conscious ArKO mice were compared with those in age- and weight-matched wild-type (WT) mice.