title: Differential adipokine response in genetically predisposed lean and obese rats during inflammation: a role in modulating experimental colitis?
abstract: 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.
authors.affiliation: Snyder Institute of Infection, Immunity and Inflammation, Hotchkiss Brain Institute and Department of Physiology and Pharmacology, University of Calgary, Calgary, Alberta, T2N 4N1, Canada.
authors.forename: Niall P
authors.initials: NP
authors.lastname: Hyland
authors.forename: Adam P
authors.initials: AP
authors.lastname: Chambers
authors.forename: Catherine M
authors.initials: CM
authors.lastname: Keenan
authors.forename: Quentin J
authors.initials: QJ
authors.lastname: Pittman
authors.forename: Keith A
authors.initials: KA
authors.lastname: Sharkey
mesh_terms: D054392:Adipokines / Q000097:blood*; D052242:Adiponectin / Q000097:blood; D000818:Animals; D001835:Body Weight / Q000187:drug effects / Q000235:genetics; D003093:Colitis, Ulcerative / Q000097:blood* / Q000139:chemically induced / Q000150:complications / Q000473:pathology / Q000503:physiopathology*; D003106:Colon / Q000187:drug effects / Q000201:enzymology / Q000473:pathology; D004435:Eating / Q000187:drug effects / Q000235:genetics; D017097:Electric Impedance; D055724:Electrophysiological Phenomena / Q000187:drug effects / Q000502:physiology; D020022:Genetic Predisposition to Disease; D054439:Ghrelin / Q000097:blood; D007249:Inflammation / Q000097:blood* / Q000139:chemically induced / Q000150:complications / Q000503:physiopathology; D007328:Insulin / Q000097:blood; D020738:Leptin / Q000097:blood; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009765:Obesity / Q000097:blood* / Q000150:complications / Q000235:genetics / Q000503:physiopathology*; D009195:Peroxidase / Q000378:metabolism; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood / Q000235:genetics; D051381:Rats; D011919:Rats, Inbred Strains; D058258:Serpin E2; D015843:Serpins / Q000235:genetics; D013851:Thinness / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D014302:Trinitrobenzenesulfonic Acid / Q000008:administration & dosage / Q000494:pharmacology
chemical_list: D054392:Adipokines; D052242:Adiponectin; D054439:Ghrelin; D007328:Insulin; D020738:Leptin; D017395:Plasminogen Activator Inhibitor 1; D058258:Serpin E2; C511869:Serpine2 protein, mouse; D015843:Serpins; D014302:Trinitrobenzenesulfonic Acid; D009195:Peroxidase