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Volume 11 (2011), Pages 2197-2206
Research Article

Subcutaneous Adipose Tissue from Obese and Lean Adults Does Not Release Hepcidin In Vivo

1USDA Agricultural Research Service, Louisiana State University AgCenter, Knapp Hall, Baton Rouge, LA 70803, USA
2Oxford Center for Diabetes, Endocrinology and Metabolism, University of Oxford, Churchill Hospital, Oxford OX3 7LJ, UK
3The Translational Research Institute for Metabolism and Diabetes 2566 Lee Rd, Winter Park, FL 32789, USA
4Intrinsic LifeSciences LLC, La Jolla, CA 92037, USA
5University of Oxford and NIHR Oxford Biomedical Research Centre, Oxford OX3 7LJ, UK
6Division of Pulmonary and Critical Care Medicine, David Geffen School of Medicine, University of California at Los Angeles, 10833 Le Conte Avenue, Los Angeles, CA 90095, USA
7Department of Kinesiology and Nutrition, University of Illinois at Chicago, 1919 W. Taylor Street, Room 650, Chicago, IL 60612, USA

Received 14 July 2011; Accepted 23 September 2011

Academic Editor: Giamila Fantuzzi

Copyright © 2011 Lisa Tussing-Humphreys et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Hepcidin is the main regulator of systemic iron homeostasis and is primarily produced by the liver but is also expressed, at the mRNA-level, in periphery tissues including the subcutaneous and visceral adipose tissue. Obesity is associated with elevated hepcidin concentrations and iron depletion suggesting that the exaggerated fat mass in obesity could contribute significantly to circulating hepcidin levels consequently altering iron homeostasis. The objective of this study was to determine if abdominal subcutaneous adipose tissue (AbScAT) releases hepcidin in vivo and if release is modified by obesity. Arterio-venous differences in concentrations of hepcidin were measured across AbScAT in 9 obese and 9 lean adults. Overall ( 𝑛 = 1 8 ), mean plasma hepcidin concentrations were significantly higher in arterialized compared to AbScAT venous samples [mean difference (arterialized-AbScAT venous plasma hepcidin) = 4 . 9 ± 9 . 6  ng/mL, 𝑃 = 0 . 0 4 ]. Net regional release was not calculated because mean venous plasma hepcidin concentrations were lower than mean arterialized concentrations indicating no net release. Significant correlations between AbScAT venous and arterialized plasma hepcidin concentrations with anthropometric variables were not observed. Findings from this vein drainage study suggest there is no net release of hepcidin from the AbScAT depot and thereby no ability to signal systemically, even in obesity.