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Background: Inflammatory bowel disease (IBD) is an important cause of chronic disability in humans. Methods:We characterized a model of chronic IBD in young male Wistar rats by administering dextran sodium sulfate (DSS: 0%, 0.25%, 0.5%, or 1% in drinking water) for six weeks, with 0.5% DSS for twelve weeks, following DSS cessation or together with treatment with sulfasalazine for the last 6 weeks. We measured gastrointestinal characteristics including stool consistency, blood in stools, small intestine and colon length, intestinal transit and permeability, and gut microbiota, as well as extra-intestinal parameters including oral glucose tolerance, systolic blood pressure, fat and lean mass, and left ventricular stiffness. Results: At 6 weeks, 0.25-1% DSS produced gastrointestinal changes as diarrhea and blood in stools. At 12 weeks, 0.5% DSS produced chronic and sustained gastrointestinal changes, with marked infiltration of inflammatory cells throughout the gastrointestinal tract and crypt distortion. Firmicutes increased and Bacteroidetes and Actinobacteria decreased in DSStreated rats. Changes were reversed by DSS cessation or sulfasalazine treatment. Gastrointestinal permeability and extra-intestinal parameters did not change, so DSS changes were limited to the gastrointestinal tract. Conclusion: Chronic 0.5% DSS produces selective and reversible gastrointestinal changes, providing an improved chronic model in rats that mimics human IBD for testing new interventions.

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Osteoarthritis (OA) is a degenerative condition of joints, causing pain and swelling, and can be caused or worsened by trauma and obesity. The objectives of this study were to determine whether pain behaviour and progression of OA were increased in rats with trauma-induced OA fed dietary saturated fatty acids (SFA). Male Wistar rats were fed either a corn starch diet (C) or high-carbohydrate high-fat diet (H) with either 20% beef tallow or SFA (lauric (HLA), myristic (HMA), palmitic (HPA) or stearic (HSA) acids) for 16 weeks prior to and 8 weeks after excision of the medial meniscus of right knee joint to initiate OA when pain behaviour, glial activity, progression of knee OA, inflammatory mediators and signs of metabolic syndrome were assessed. Rats fed beef tallow, palmitic or stearic acids showed increased pain symptoms characterised by decreased hind paw/limb withdrawal thresholds and grip strengths and increased spinal astrogliosis and microgliosis compared to rats fed lauric or myristic acids. However, the severity of OA joint damage was unchanged by these dietary manipulations. We conclude that pain symptoms of trauma-induced OA in rats worsen with increased dietary beef tallow or palmitic or stearic acids, but improve with lauric or myristic acids, despite unchanged OA cartilage damage.

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