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Horm Metab Res 2002; 34(11/12): 746-751
DOI: 10.1055/s-2002-38242
Review
© Georg Thieme Verlag Stuttgart · New York

The Functional Consequences of 11β-Hydroxysteroid Dehydrogenase Expression in Adipose Tissue

J.  W.  Tomlinson1 , P.  M.  Stewart1
  • 1Division of Medical Sciences, University of Birmingham, Queen Elizabeth Hospital, Edgbaston, Birmingham, UK
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Received 1 October 2002

Accepted after revision 6 November 2002

Publikationsdatum:
27. März 2003 (online)

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Abstract

Clinical observations have highlighted the link between glucocorticoids and obesity. While exogenous glucocorticoids in excess predispose to the development of central obesity, we have focused on cortisol metabolism within human adipose tissue. 11β-hydroxysteroid dehydrogenase (11β-HSD) inter-converts the active glucocorticoid, cortisol, and inactive cortisone. 11β-HSD1, the only isoform expressed in adipose tissue, acts predominantly as an oxoreductase to generate cortisol. Expression is higher in omental compared to subcutaneous preadipocytes and activity and expression are potently regulated by growth factors and cytokines. Mice over-expressing 11β-HSD1 specifically within adipocytes develop central obesity. However, the situation is less clear in humans. Globally, there appears to be inhibition of the enzyme, but expression in human obesity is still not fully characterized; its functional role in adipocyte biology remains to be elucidated. In vitro, 11β-HSD1 appears to function in promoting adipocyte differentiation and limiting preadipocyte proliferation, but the impact of these effects in vivo upon the regulation of fat mass remains to be defined. Clinical studies utilizing selective 11β-HSD1 inhibitors may help to answer this question.

Key words

11β-Hydroxysteroid Dehydrogenase - Obesity - Adipose Tissue - Proliferation - Differentiation - Cortisol - Preadipocyte

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Prof. P. M. Stewart, M.D., F.R.C.P., F.Med.Sci.

Division of Medical Sciences

University of Birmingham · Queen Elizabeth Hospital · Birmingham · United Kingdom B15 2TH ·

Telefon: + 44 (121) 627 2380

Fax: + 44 (121) 121 627 2384

eMail: P.M.Stewart@bham.ac.uk