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Role of metabolically active hormones in the insulin resistance associated with short-term glucocorticoid treatment

Jeetesh V Patel1, David E Cummings2, John P Girod3, Alwin V Mascarenhas1, Elizabeth A Hughes1, Manjula Gupta4, Gregory YH Lip1, Sethu Reddy4 and Daniel J Brotman4*

Author Affiliations

1 Haemostasis Thrombosis and Vascular Biology Unit, University Department of Medicine and Sandwell Medical Research Unit, Sandwell and West Birmingham Hospitals NHS Trust, West Midlands, UK

2 Department of Medicine, University of Washington, Veterans Affairs Puget Sound Health Care System, Seattle, WA, USA

3 Department of Cardiology, University of Pittsburgh Medical Center, Pittsburgh, PA, USA

4 Departments of General Internal Medicine and Endocrinology, Diabetes and Metabolism, Cleveland Clinic Foundation, Cleveland, OH, USA

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Journal of Negative Results in BioMedicine 2006, 5:14  doi:10.1186/1477-5751-5-14

Published: 11 September 2006



The mechanisms by which glucocorticoid therapy promotes obesity and insulin resistance are incompletely characterized. Modulations of the metabolically active hormones, tumour necrosis factor alpha (TNF alpha), ghrelin, leptin and adiponectin are all implicated in the development of these cardiovascular risk factors. Little is known about the effects of short-term glucocorticoid treatment on levels of these hormones.

Research methods and procedures

Using a blinded, placebo-controlled approach, we randomised 25 healthy men (mean (SD) age: 24.2 (5.4) years) to 5 days of treatment with either placebo or oral dexamethasone 3 mg twice daily. Fasting plasma TNF╬▒, ghrelin, leptin and adiponectin were measured before and after treatment.


Mean changes in all hormones were no different between treatment arms, despite dexamethasone-related increases in body weight, blood pressure, HDL cholesterol and insulin. Changes in calculated indices of insulin sensitivity (HOMA-S, insulin sensitivity index) were strongly related to dexamethasone treatment (p < 0.001).


Our data do not support a role for TNF alpha, ghrelin, leptin or adiponectin in the insulin resistance associated with short-term glucocorticoid treatment.