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The Journal of Clinical Endocrinology & Metabolism Vol. 86, No. 6 2817-2825
Copyright © 2001 by The Endocrine Society

Other Original Studies

Dexamethasone Inhibits Tumor Necrosis Factor-{alpha}-Induced Apoptosis and Interleukin-1ß Release in Human Subcutaneous Adipocytes and Preadipocytes1

Hui H. Zhang2, Sudhesh Kumar, Anthony H. Barnett and Margaret C. Eggo

Division of Medical Sciences, University of Birmingham, Birmingham, United Kingdom B15 2TT

Address all correspondence and requests for reprints to: Dr. Margaret C. Eggo, The Medical School, University of Birmingham, Birmingham, United Kingdom B15 2TT. E-mail: m.c.eggo{at}.bham.ac.uk

Abstract

Tumor necrosis factor-{alpha} (TNF{alpha}) can decrease adipose tissue mass, but in obesity, adipose tissue hypertrophy persists despite increased TNF{alpha} expression. The hormonal milieu of obesity may antagonize the adipostat effects of TNF{alpha}. We examined the effects of insulin and the synthetic glucocorticoid, dexamethasone (Dex), on TNF{alpha}-induced apoptosis and gene expression in human adipocytes and preadipocytes. Using RT multiplex PCR, the expression of the proapoptotic genes interleukin-1ß (IL-1ß)-converting enzyme (ICE) and TNF{alpha} and the antiapoptotic genes bcl-2, nuclear factor-{kappa}B (NF{kappa}B), and NF{kappa}B inhibitory subunit, I{kappa}B, were examined. The expression and release of IL-1ß, a postulated downstream effector of ICE-mediated apoptosis, were also determined. TNF{alpha} increased the messenger ribonucleic acid levels of ICE, TNF{alpha}, IL-1ß, bcl-2, and NF{kappa}B in preadipocytes and adipocytes (P < 0.01). Dex inhibited TNF{alpha}-induced messenger ribonucleic acid expression of ICE, TNF{alpha}, and IL-1ß (P < 0.01), but not that of bcl-2 and NF{kappa}B. TNF{alpha} stimulated IL-1ß release from preadipocytes and adipocytes up to 20-fold, but the effect was abrogated by Dex. Apoptosis induced by TNF{alpha} was reduced to control levels (P < 0.01) by Dex. Insulin had no significant effect on TNF{alpha}-induced apoptosis and gene expression. In obesity, glucocorticoids may reduce TNF{alpha} actions in adipose tissue by inhibiting TNF{alpha}-induced apoptosis, IL-1ß release, and TNF{alpha} expression.




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