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This Article Full Text Full Text (PDF) All Versions of this Article: 297/5/G869    most recent 00164.2009v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Hyland, N. P. Articles by Sharkey, K. A. PubMed PubMed Citation Articles by Hyland, N. P. Articles by Sharkey, K. A.

INFLAMMATION/IMMUNITY/MEDIATORS

Differential adipokine response in genetically predisposed lean and obese rats during inflammation: a role in modulating experimental colitis?

¹Snyder Institute of Infection, Immunity and Inflammation, Hotchkiss Brain Institute and Department of Physiology and Pharmacology, University of Calgary, Calgary, Alberta, Canada; ²Alimentary Pharmabiotic Centre and Department of Pharmacology and Therapeutics, University College Cork, Cork, Ireland

Submitted April 30, 2009 ; accepted in final form September 3, 2009

The relationship between a predisposition to obesity and the development of colitis is not well understood. Our aim was to characterize the adipokine response and the extent of colitis in diet-induced obese (DIO) rats. DIO and control, diet-resistant (DR) animals were administered either saline or trinitrobenzene sulfonic acid (TNBS) to induce colitis. Macroscopic damage scores and myeloperoxidase (MPO) activity were measured to determine the extent of inflammation. Trunk blood was collected for the analysis of plasminogen activator inhibitor-1 (PAI-1) as well as leptin, ghrelin, and adiponectin. Colonic epithelial physiology was assessed using Ussing chambers. DIO rats had a modestly increased circulating PAI-1 before TNBS treatment; however, during colitis, DR animals had more than a fourfold increase in circulating PAI-1 compared with DIO rats. Circulating leptin was higher in DIO rats compared with DR animals, in the inflamed and noninflamed states. These changes in TNBS-induced adipokine profile were accompanied by decreased macroscopic tissue damage score in DIO animals compared with DR tissues. Furthermore, TNBS-treated DR animals lost significantly more weight than DIO rats during active inflammation. Colonic epithelial physiology was comparable between groups, as was MPO activity. The factors contributing to the decreased colonic damage are almost certainly multifold, driven by both genetic and environmental factors, of which adipokines are likely to play a part given the increasing body of evidence for their role in modulating intestinal inflammation.

diet-induced obese; body weight; leptin; plasminogen activator inhibitor-1; adiponectin; ghrelin