Obesity and corticosteroids: 11 beta-Hydroxysteroid type 1 as a cause and therapeutic target in metabolic disease

Research output: Contribution to journalLiterature reviewpeer-review


The metabolic abnormalities found associated with high blood glucocorticoid levels (e.g. rare Cushing's syndrome) include insulin-resistance, visceral obesity, hypertension, dyslipidaemia and an increased risk of cardiovascular diseases. The same constellation of abnormalities is found in the highly prevalent idiopathic obesity/insulin-resistance (metabolic)-syndrome. It is now apparent that tissue-specific changes in cortisol metabolism explain these parallels rather than altered blood cortisol levels. Primary among these changes is increased intracellular glucocorticoid reactivation, catalysed by the enzyme 11 beta-hydroxysteroid dehydrogenase type (HSD)-1 in obese adipose tissue. Liver, skeletal muscle, endocrine pancreas, blood vessels and leukocytes express 11 beta-HSD1 and their potential role in metabolic disease is discussed. The weight of evidence, much of it gained from animal models, suggests that therapeutic inhibition of 11 beta-HSD1 will be beneficial in most cellular contexts, with clinical trials supportive of this concept. (C) 2009 Elsevier Ireland Ltd. All rights reserved.

Original languageEnglish
Pages (from-to)154-164
Number of pages11
JournalMolecular and Cellular Endocrinology
Issue number2
Publication statusPublished - 25 Mar 2010


  • Obesity
  • Glucocorticoid
  • 11-hydroxysteroid
  • adipose
  • Insulin-resistance
  • Therapy

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