Sepsis-Induced Adipokine Change with regard to Insulin Resistance. (9th January 2012)

• Record Type: Journal Article
• Authors: Hillenbrand, Andreas; Weiss, Manfred; Knippschild, Uwe; Wolf, Anna Maria; Huber-Lang, Markus
• Other Names: Kaski Juan Carlos Academic Editor.
• Is Part Of: International journal of inflammation. Volume 2012(2012)
• Publication Date: 2012-01-09
• Subjects: Inflammation -- Periodicals; Inflammation; Inflammation; Periodicals; 617.22
• DOI: 10.1155/2012/972368
• Languages: English
• ISSNs: 2090-8040

Abstract

Abstract : 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.