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Resistin Is More Abundant in Liver Than Adipose Tissue and Is Not Up-Regulated by Lipopolysaccharide

Departments of Medical Biomics (E.S., R.J.V.), and Pharmacokinetics and Drug Delivery (M.G.L.E., G.M.M.G.), University of Groningen, University Medical Centre Groningen (UMCG), 9713 AV Groningen, The Netherlands; and Department of Obstetrics and Gynecology (A.H.), University of Groningen, UMCG, 9700 RB Groningen, The Netherlands

Address all correspondence and requests for reprints to: Ewa Szalowska, M.Sc., Department of Medical Biomics, University of Groningen, University Medical Centre Groningen, Antonius Deusinglaan 1, 9713 AV Groningen, The Netherlands. E-mail: e.szalowska{at}med.umcg.nl.

Context: Resistin is an adipokine correlated with inflammatory markers and is predictive for cardiovascular diseases. There is evidence that serum resistin levels are elevated in obese patients; however, the role of resistin in insulin resistance and type 2 diabetes remains controversial.

Objective: We addressed the question of whether inflammation may induce expression of resistin in organs involved in regulation of total body energy metabolism, such as liver and adipose tissue (AT).

Methods: Human liver tissue, sc AT, and omentum were cultured in the absence/presence of lipopolysaccharide (LPS). The resistin and cytokine mRNA and protein expression levels were determined by real-time PCR, ELISA, and Multiplex Technology, respectively. The localization of resistin in human liver was analyzed by immunohistochemistry.

Results: Resistin gene and protein expression was significantly higher in liver than in AT. Exposure of human AT and liver tissue in culture to LPS did not alter resistin concentration; however, concentrations of IL-1β, IL-6, and TNF were significantly increased in these tissues. In liver, resistin colocalizes with markers for Kupffer cells, for a subset of endothelial and fibroblast-like cells.

Conclusions: High level of resistin gene and protein expression in liver compared to AT implies that resistin should not be considered only as an adipokine in humans. LPS-induced inflammation does not affect resistin protein synthesis in human liver and AT. This suggests that elevated serum resistin levels are not indicative for inflammation of AT or liver in a manner similar to known inflammatory markers such as IL-1β, IL-6, or TNF.