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Recent Progress in Hormone Research 59:359-393 (2004)
© 2004 The Endocrine Society

Glucocorticoids and 11beta-Hydroxysteroid Dehydrogenase in Adipose Tissue

Jonathan R. Seckl, Nik M. Morton, Karen E. Chapman and Brian R. Walker

Endocrinology Unit, School of Molecular and Clinical Medicine, University of Edinburgh, Western General Hospital, Edinburgh EH4 2XU, Scotland, United Kingdom

The highly prevalent metabolic syndrome (insulin resistance, type 2 diabetes, dyslipidemia, hypertension, along with abdominal obesity) resembles Cushing’s syndrome. However, in simple obesity, plasma cortisol levels are not elevated. 11beta-hydroxysteroid dehydrogenase type 1 (11ß-HSD1), at least in mature adipocytes and hepatocytes, converts inactive circulating 11-keto steroids into active glucocorticoids, amplifying local glucocorticoid action. 11ß-HSD1 is elevated in adipose tissue in obese humans and rodents, suggesting that adipose tissue glucocorticoid excess may explain the conundrum. Indeed, transgenic mice overexpressing 11ß-HSD1 in adipose tissue faithfully replicate the metabolic syndrome. Conversely, 11ß-HSD1-/- mice resist the metabolic consequences of stress and high-fat feeding via insulin sensitisation and other advantageous effects in the liver and adipose tissue. Adipose 11ß-HSD1 deficiency contributes to a protective metabolic phenotype, supporting its role as a therapeutic target for the metabolic syndrome.




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