Effects of fructan source and degree of polymerization on intestinal barrier function and histomorphology characteristics in obese C57BL/6 mice

solute carrier family 5, member 8 (SLC5A8);monocarboxylic transporter-1 (MCT-1);monocarboxylic transporter-4(MCT-4);solute carrier family 5, member 12(SLC5A12);"5 AMP-activated protein kinase (AMPK)";G-protein coupled receptor-43 (GPR43);mucin 2 (MUC2);zonula occluden-1(ZO-1);taste receptor type 2-38 (T2R38);obesity and intestinal barrier function;obesity and gut permeability;obesity;obese rodent model;inflammation;fructan prebiotics;inulin;short-chain fructooligosaccharides (scFOS);crypt depth;villus height

Cephas, Kimberly ; Swanson ; Kelly S.

关键词: solute carrier family 5, member 8 (SLC5A8);    monocarboxylic transporter-1 (MCT-1);    monocarboxylic transporter-4(MCT-4);    solute carrier family 5, member 12(SLC5A12);    "5 AMP-activated protein kinase (AMPK)";    G-protein coupled receptor-43 (GPR43);    mucin 2 (MUC2);    zonula occluden-1(ZO-1);    taste receptor type 2-38 (T2R38);    obesity and intestinal barrier function;    obesity and gut permeability;    obesity;    obese rodent model;    inflammation;    fructan prebiotics;    inulin;    short-chain fructooligosaccharides (scFOS);    crypt depth;    villus height;   

Others  :  https://www.ideals.illinois.edu/bitstream/handle/2142/32026/Cephas_Kimberly.pdf?sequence=1&isAllowed=y

美国|英语

来源: The Illinois Digital Environment for Access to Learning and Scholarship

【 摘 要 】

Obesity is linked to increased intestinal permeability that may contribute to low grade inflammation. Fructan prebiotics have been demonstrated to increase intestinal resistance and decrease systemic inflammation. The objective of this study was to test the effects of prebiotics on intestinal permeability, morphology, and gene expression in an obese mouse model. Obese, 18-wk old, C57BL/6 mice were randomized to high-fat (45% of kcal) diets containing 5% cellulose, 10% cellulose, 10% short-chain fructooligosaccharides (scFOS) or 10% inulin and fed for 28 d. Distal ileum, cecum, and colon samples were collected for Ussing chamber, histomorphology, and qRT-PCR analyses. The effects of treatment were tested using the Mixed Models procedure of SAS. Among treatments, mice fed scFOS and inulin had greater (p<0.05) intestinal transmural resistance compared to mice fed 5% cellulose. MCT-1 expression was greater (p<0.05) in the distal colon of mice fed 10% cellulose compared to 10% inulin. ZO-1 expression was lower (p<0.05) in mice fed inulin compared to other treatments. Occludin mRNA abundance was lowest (p<0.05) in fructan sources compared to cellulose. When comparing 5% vs. 10% cellulose treatments using contrasts, 10% cellulose led to greater (p<0.05) intestinal crypt depth in all intestinal regions, except the distal colon.Mice fed 5% vs. 10% cellulose, however, had greater (p<0.05) ileal villus height: crypt depth ratio, ileal MUC2 mRNA abundance, proximal colon AMPK mRNA abundance, and occludin mRNA abundance in the proximal and distal colon regions. When comparing fructan vs. cellulose treatments using contrasts, fructans resulted in a greater (p<0.05) transmural resistance and crypt depth when all intestinal regions were combined.In contrast, fructan-fed mice had lower (p<0.05) mRNA abundance of ZO-1 and occludin when all intestinal regions were combined (Table 3.5). Fructan consumption resulted in lower (p<0.05) ileal MUC2 and occludin mRNA abundance, cecal occludin mRNA abundance, proximal colon MCT-1, ZO-1, AMPK, and occludin mRNA abundance, and distal colon ZO-1, AMPK, and occludin mRNA abundance.Cecal AMPK mRNA abundance was greater (p<0.05) in fructan-fed compared to cellulose-fed mice.Pearson coefficient correlations indicated correlations between MCT-1 and distal colon ZO-1 (r = 0.77, p<0.05) and occludin mRNA abundance (r = 0.66, p<0.05). AMPK correlated with ZO-1 mRNA abundance (r = > 0.60, p<0.05) in all regions of the intestinal tissue of C57BL/6 mice. Lastly, ZO-1 mRNA abundance correlated with distal colon epithelial resistance (r = 0.51, p<0.05). Collectively, these data may suggest mechanisms by which equivalent quantities of fructan prebiotics and non-fermentable fibers affect intestinal barrier function.