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Lancet. 1997 Apr 26;349(9060):1210-3.

Does central obesity reflect "Cushing's disease of the omentum"?

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  • 1Department of Medicine, University of Birmingham, Queen Elizabeth Hospital, Edgbaston, UK.

Abstract

BACKGROUND:

Central obesity results in a cluster of metabolic abnormalities contributing to premature death. Glucocorticoids regulate adipose-tissue differentiation, function, and distribution, and in excess, cause central obesity. Glucocorticoid hormone action is, in part, controlled by two isoforms of the enzyme 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD) which interconverts hormonally active cortisol to inactive cortisone. We studied cortisol metabolism within different adipose tissue depots.

METHODS:

We analysed expression and activity of the two isoforms (1 and 2) of 11 beta-HSD in cultured omental and subcutaneous adipose stromal cells from 16 patients undergoing elective abdominal surgery.

FINDINGS:

Only the type 1 isoform (11 beta-HSD1) was expressed in adipose stromal cells. The predominant activity was oxo-reductase (conversion of cortisone to cortisol greater than cortisol to cortisone) and was higher in omental than subcutaneous fat (cortisone to cortisol, median 57.6 pmol mg-1 h-1 [95% CI 25.8-112.9] vs 0 pmol mg-1 h-1 [0-0.6], p < 0.001). 11 beta-HSD1 oxo-reductase activity was further increased (127.5 pmol mg-1 h-1 [82.1-209], p < 0.05) when omental adipose stromal cells were treated with cortisol and insulin.

INTERPRETATION:

Adipose stromal cells from omental fat, but not subcutaneous fat, can generate active cortisol from inactive cortisone through the expression of 11 beta-HSD1. The expression of this enzyme is increased further after exposure to cortisol and insulin. In vivo, such a mechanism would ensure a constant exposure of glucocorticoid specifically to omental adipose tissue, suggesting that central obesity may reflect "Cushing's disease of the omentum".

PMID:
9130942
[PubMed - indexed for MEDLINE]
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