Horm Metab Res 2002; 34(11/12): 698-702
DOI: 10.1055/s-2002-38257
Original Clinical
© Georg Thieme Verlag Stuttgart · New York

Glucocorticoid-Regulated Adipose Tissue Secretion of PAI-1, but not IL-6, TNFα or Leptin in Vivo

J.  Uddén 1 , P.  Eriksson 2 , J.  Hoffstedt 1
  • 1 Centre for metabolism and Endocrinology, Huddinge University Hospital, Stochholm, Sweden
  • 2 Atherosclerosis Research Unit, King Gustaf V Research Institute, Karolinska Institute, Karolinska Hospital, Stockholm, Sweden
Further Information

Publication History

Received 1 October 2002

Accepted after revision 26 November 2002

Publication Date:
27 March 2003 (online)

Abstract

Objective: Glucocorticoids are well-known regulators of adipose tissue metabolism and endocrine function. The aim of this study was to examine glucocorticoid effect on plasminogen activator inhibitor 1 (PAI-1), tumour necrosis factor alpha (TNFα), leptin and interleukin-6 (IL-6) adipose tissue secretion. Material and Methods: Twelve healthy postmenopausal women with mean BMI of 28.9 kg/m² (± 0.8 SEM) received 25 mg prednisolone daily for 7 days. Before and after glucocorticoid treatment adipose tissue secretion of PAI-1, leptin, IL-6 and TNFα were measured, and adipocyte PAI-1 mRNA as well as anthropometrical and bio-chemical data were obtained. Results: Anthropometric measurements remained unaffected. Analyses of venous blood-samples showed a borderline increase of insulin levels (p = 0.062). PAI-1 secretion from adipose tissue increased (1.9 ± 0.2 vs. 3.5 ± 0.5 ng/g triglycerides, p = 0.012), but PAI-1 mRNA levels did not (0.19 ± 0.02 vs. 0.21 ± 0.04 arbitrary units after normalised to β-actin, p = 0.51). There were no apparent differences in IL-6, TNFα or leptin secretion after glucocorticoid exposure. Conclusion: This study shows an increased secretion of PAI-1, but not IL-6, TNFα or leptin, from abdominal adipose tissue after in vivo glucocorticoid treatment, which may be a finding of pathophysiological importance given the well-known effect of glucocorticoid excess on metabolic aberrations and cardiovascular morbidity.

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J. Hoffstedt, M.D., Ph.D.

Karolinska Institutet

M61, CME · Huddinge University Hospital · 141 86 Stockholm · Sweden ·

Phone: + 46 (8) 58 58 00 00

Email: johan.hoffstedt@medhs.ki.se

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