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International Journal of Inflammation
Volume 2012 (2012), Article ID 972368, 7 pages
Review Article

Sepsis-Induced Adipokine Change with regard to Insulin Resistance

1Department of General, Visceral, and Transplantation Surgery, University Hospital of Ulm, Steinhoevelstraße 9, 89075 Ulm, Germany
2Clinic of Anesthesiology, University Hospital of Ulm, Steinhoevelstraße 9, 89075 Ulm, Germany
3Department of Traumatology, Hand and Reconstructive Surgery, University Hospital of Ulm, Steinhoevelstraße 9, 89075 Ulm, Germany

Received 12 June 2011; Revised 22 September 2011; Accepted 5 October 2011

Academic Editor: Juan Carlos Kaski

Copyright © 2012 Andreas Hillenbrand 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.


Background. Assessment of white adipose tissue has changed in recent years, with WAT now being considered as an active endocrine organ, secreting a large number of bioactive mediators, so-called adipokines. Besides other functions, these adipokines are involved in inflammatory response thereby exhibiting predominantly proinflammatory or anti-inflammatory properties and contribute to insulin resistance. Methods. Comprehensive review of the literature of the role of adipokines relevant to critical care medicine using PubMed search. Results. Adiponectin—the prototype of an anti-inflammatory and insulin-sensitizing adipokine—is diminished in sepsis, while resistin—a protein with proinflammatory properties—is elevated. Plasminogen activator inhibitor-1, interleukin (IL)-1, IL-6, IL-8, and IL-10, and tumor-necrosis-factor-alpha mediate insulin resistance and are elevated in sepsis, while retinol-binding protein-4 concentrations are significantly reduced in sepsis. Chemerin displays potent anti-inflammatory and insulin-resistance properties, while monocyte chemotactic protein-1—increased in sepsis—contributes to macrophage infiltration in adipose tissue and insulin resistance. Conclusions. The expression of adipokines in humans is altered as well in obese as in septic patients with elevated levels of proinflammatory adipokines. Changes in adipokine levels in acute sepsis could contribute to insulin resistance. Consequently, in critically ill patients, these alterations underline a possible contribution of adipokines in the development of hyperglycemia.