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The Journal of Clinical Endocrinology & Metabolism Vol. 86, No. 3 1418-1421
Copyright © 2001 by The Endocrine Society

Rapid Communications

Tissue-Specific Dysregulation of Cortisol Metabolism in Human Obesity

Eva Rask, Tommy Olsson, Stefan Soderberg, Ruth Andrew, Dawn E. W. Livingstone, Owe Johnson and Brian R. Walker

Departments of Public Health and Clinical Medicine (E.R., T.O., SS., O.J.), Ume University Hospital, Ume, Sweden; and Department of Medical Sciences (R.A., D.E.W.L., B.R.W.), University of Edinburgh, Western General Hospital, Edinburgh, United Kingdom

Address correspondence to: Brian R. Walker, M.D., Department of Medical Sciences, Endocrinology Unit, The University of Edinburgh, Western General Hospital, EH4 2XU Edinburgh, United Kingdom.

Abstract

Cortisol has been implicated as a pathophysiological mediator in idiopathic obesity, but circulating cortisol concentrations are not consistently elevated. The tissue-specific responses to cortisol may be influenced as much by local prereceptor metabolism as by circulating concentrations. For example, in liver and adipose tissue cortisol is regenerated from inactive cortisone by 11ß-hydroxysteroid dehydrogenase type 1 (11ß-HSD1). In obese Zucker rats 11ß-HSD1 activity is reduced in liver but enhanced in adipose tissue. This study addressed whether the same tissue-specific disruption of cortisol metabolism occurs in human obesity. 34 men were recruited from the MONICA population study in Northern Sweden to represent a wide range of body composition and insulin insensitivity. Plasma cortisol was measured at 0830h and 1230h, after overnight low-dose dexamethasone suppression, after intravenous corticotropin releasing hormone (CRH), and after oral cortisone administration. Urinary cortisol metabolites were measured in a 24 h sample. A subcutaneous fat biopsy was obtained from 16 participants to measure cortisol metabolism in vitro. Higher body mass index was associated with increased total cortisol metabolite excretion (r = 0.47, p < 0.01), but lower plasma cortisol at 1230 h and after dexamethasone, and no difference in response to CRH. Obese men excreted a greater proportion of glucocorticoid as metabolites of cortisone rather than cortisol (r = 0.43, p < 0.02), and converted less cortisone to cortisol after oral administration (r = 0.49, p < 0.01), suggesting impaired hepatic 11ß-HSD1 activity. By contrast, in vitro 11ß-HSD1 activity in subcutaneous adipose tissue was markedly enhanced in obese men (r = 0.66, p < 0.01). We conclude that in obesity, reactivation of cortisone to cortisol by 11ß-HSD1 in liver is impaired, so that plasma cortisol levels tend to fall, and there may be a compensatory increase in cortisol secretion mediated by a normally functioning hypothalamic-pituitary-adrenal axis. However, changes in 11ß-HSD1 are tissue-specific: strikingly enhanced reactivation of cortisone to cortisol in subcutaneous adipose tissue may exacerbate obesity; and it may be beneficial to inhibit this enzyme in adipose tissue in obese patients.




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