Background A Western diet (WD) is associated with increased inflammation in the large intestine, which is often ascribed to the high dietary fat content. Intestinal inflammation in rodents can be induced by oral administration of dextran sulfate sodium (DSS). However, most studies investigating effects of WD and DSS have not used appropriate low-fat diets as control. Objective To compare the effects of a WD with those of a low-fat-diet (LFD), on colon health in a DSS-induced low-grade colonic inflammation mouse model. Methods Six-week old male C57BL/6JRj mice were fed a LFD (fat = 10.3% energy, n = 24) or a WD (fat = 41.2% energy, n = 24) for 15 weeks (Exp.1). Half the mice on each diet (n = 12) then received 1% DSS in water for six days with the remaining (n = 24) administered water. Disease activity, proinflammatory genes, inflammatory biomarkers and fecal microbiota (16S rRNA) were assessed (Exp.1). Follow-up experiments (Exp.2 and Exp.3), were performed to investigate whether fat source (milk or lard; Exp.2) affected outcomes and whether a shift from LFD to WD one day prior to 1% DSS exposure caused an immediate effect on DSS-induced inflammation (Exp.3). Results In Exp.1, 1% DSS treatment significantly increased disease score in the LFD group compared with the WD group (2.7 vs 0.8, P<0.001). Higher levels of fecal lipocalin (11-fold, P<0.001), proinflammatory gene expression (up to 82-fold) and Proteobacteria were observed in LFD-fed mice compared with WD group. The two fat sources in WDs (Exp.2) revealed the same low inflammation in WD+DSS compared to LFD+DSS mice. Finally, the switch from LFD to WD just before DSS exposure resulted in reduced colonic inflammation (Exp.3). Conclusions Herein, WDs (with milk or lard) protected mice against DSS-induced colonic inflammation compared with LFD-fed mice. Whether fat intake induces protective mechanisms against DSS mediated inflammation or inhibits establishment of the DSS-induced colitis model is unclear.

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Rodent studies have shown that legumes can reduce chemical induced colonic inflammation, but the role of faba bean fractions for colon health has not been described. We have investigated the role of protein and fiber fractions of faba beans for colonic health and microbiota composition in a low-grade inflammation mice-model when incorporated in a Western diet (WD). The diet of sixty C57BL/6JRj male mice was standardized to a WD (41% fat, 43% carbohydrates) before were randomly assigned to four groups (n = 12) receiving either 1) WD with 30% of the protein replaced with faba-bean proteins, 2) WD with 7% of the fiber replaced with faba-bean fibers, 3) WD with protein and fiber fractions or 4) plain WD (n = 24). Low-grade inflammation was induced by 1% dextran sodium sulfate (DSS) given to mice for the last six days of the trial. Half (n = 12) in group 4) were given only water (controls). Prior to DSS, body weight, energy intake, glucose and insulin tolerance assays were performed. Inflammatory status in the colon was assessed by biomarkers of inflammation and qRT-PCR analyses of inflammatory related genes. Fecal microbiota composition was assessed by 16S rRNA gene sequencing. 1% DSS treatment increased levels in fecal lipocalin-2 and induced disease activity index score, but the presence of faba bean fractions in WD did not influence these indicators nor the expression level of inflammatory associated genes. However, the mice that had faba-bean proteins had a lower amount of Proteobacteria compared the group on plain WD. The Actinobacteria abundance was also lower in the group that had fiber fraction from faba-beans. Overall, outcomes indicated that in a low-grade inflammation model, replacement of protein and or fiber in a WD with faba bean fractions had marginal effects on inflammatory parameters and colonic microbiota.