Xylooligosaccharide Modulates Gut Microbiota and Alleviates Colonic Inflammation Caused by High Fat Diet Induced Obesity

Abstract

Obesity leads to colonic inflammation and may increase the risk of colorectal cancer. Xylooligosaccharide (XOS) exhibits strong antioxidant and excellent antibacterial properties, and can be utilized by gut microbes to maintain the ecological balance of the intestinal tract. In this study, we explored how XOS modulates the microbiota and regulates high fat diet (HFD) induced inflammation. We measured the changes in body weight and visceral coefficients in rats fed a high-fat diet. We also measured the expression levels of inflammatory factors in the plasma and colonic tissues of the rats using the enzyme-linked immunosorbent assay and real-time quantitative polymerase chain reaction. We analyzed the composition of fecal microorganisms and short chain fatty acid (SCFA) content using 16S rDNA and GC-MS. We found that XOS significantly counteracted HFD induced weight gain. Moreover, the plasma levels of monocyte chemoattractant protein-1, tumor necrosis factor (TNF-α) and lipopolysaccharide decreased in the XOS-treated rats. XOS treatment decreased TNF-α mRNA expression and increased occludin mRNA expression in the rat colon. We observed a reduction in the overall microbial abundance in the feces of the XOS-treated rats, although the proportion of Bacteroidetes/Firmicutes increased significantly and the number of beneficial bacteria increased in the form of dominant microbes. We found that both SCFA-producing bacteria and SCFA content increased in the gut of the XOS-treated rats. We identified a correlation between the abundance of Prevotella and Paraprevotella and SCFA content. Taken together, we propose that XOS can alleviate colonic inflammation by regulating gut microbial composition and enhancing SCFA content in the gut.

Keywords: SCFA; colon inflammation; gut microbiota; high-fat diet; obesity.

FIGURE 1

Effects of HFD and XOS on body weight of rats. (A) The process of treatment, (B) body weight changes. Data are given as mean ± SD (n = 10), ^{a, b, c}mean values with different letters are significantly different from each other (P < 0.05).

FIGURE 2

Representative colon HE staining results. The colonic tissues of NC rats (A), HFD rats (B), (a: crypt injury, b: intestinal edema of the colonic mucosa, and c: intestinal edema of the colonic mucosa), and HFD + XOS rats (C) were imaged at 20× magnification. (D) Histological score. The liver tissues of NC rats (E), HFD rats (F), and HFD + XOS rats (G) were imaged at 20× magnification. Data are given as mean ± SD (n = 10), *P < 0.05.

FIGURE 3

Impact of XOS treatment on the expression of plasma inflammatory cytokines. The levels of TNF-α (A), MCP-1 (B), IL-6 (C), IL-10 (D), and LPS (E) were determined. Data are given as mean ± SD (n = 10), *P < 0.05.

FIGURE 4

Impact of XOS treatment on the expression of colonic inflammatory cytokines. The relative gene expression levels for TNF-α (A), MCP-1 (B), OCLN (C), IL-10 (D), and IL-6 (E) were determined using RT-PCR. Data are given as mean ± SD (n = 10), *P < 0.05.

FIGURE 5

Principal component analysis (PCA) score plot based on the OTU abundance. NC, normal control group; HFD, high fat diet group; HFD + XOS, XOS plus high fat diet (n = 5).

FIGURE 6

Microbial composition analysis. Taxonomic composition of the fecal bacterial communities at the phylum level (A). Taxonomic composition of the fecal bacterial communities at the genus level (B). Data are given as mean ± SD (n = 5), *P < 0.05.

FIGURE 7

Determination of fecal SCFA content and its correlation with abundance of microorganisms. The levels of acetic acid (A), propionic acid (B), isobutyric acid (C), butyric acid (D), isovaleric acid (E), and valeric acid (F) were determined. The correlation between Prevotella and acetic acid (G), the correlation between Bacteroidetes and acetic acid (H) and the correlation between Lactobacillus and acetic acid (I) were analyzed. Data are given as mean ± SD (n = 5), *P < 0.05.