Inhibition of 11beta-hydroxysteroid dehydrogenase type 1 activity in vivo limits glucocorticoid exposure to human adipose tissue and decreases lipolysis.

@article{Tomlinson2007InhibitionO1,
  title={Inhibition of 11beta-hydroxysteroid dehydrogenase type 1 activity in vivo limits glucocorticoid exposure to human adipose tissue and decreases lipolysis.},
  author={J W Tomlinson and Mark Sherlock and Beverley Hughes and Susan V. Hughes and Fiona Kilvington and William Bartlett and Rachel Courtney and Paul A. Rejto and William Carley and P. M. Stewart},
  journal={The Journal of clinical endocrinology and metabolism},
  year={2007},
  volume={92 3},
  pages={857-64}
}
CONTEXT The pathophysiological importance of glucocorticoids (GCs) is exemplified by patients with Cushing's syndrome who develop hypertension, obesity, and insulin resistance. At a cellular level, availability of GCs to the glucocorticoid and mineralocorticoid receptors is controlled by the isoforms of 11beta-hydroxysteroid dehydrogenase (11beta-HSD). In liver and adipose tissue, 11beta-HSD1 converts endogenous, inactive cortisone to active cortisol but also catalyzes the bioactivation of the… CONTINUE READING