Open AccessA high‑fructose diet induces epithelial barrier dysfunction and exacerbates the severity of dextran sulfate sodium‑induced colitis
Author(s) -
Katsuto Kawabata,
Shuji Kanmura,
Yuko Morinaga,
Akihito Tanaka,
T. Makino,
Tomohiro Fujita,
Shiho Arima,
Fumisato Sasaki,
Yuichiro Nasu,
Shiroh Tanoue,
Shinichi Hashimoto,
Akio Ido
Publication year - 2018
Publication title -
international journal of molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.048
H-Index - 90
eISSN - 1791-244X
pISSN - 1107-3756
DOI - 10.3892/ijmm.2018.4040
Subject(s) - occludin , barrier function , medicine , colitis , inflammatory bowel disease , fructose , tumor necrosis factor alpha , endocrinology , gut flora , gastroenterology , tight junction , immunology , chemistry , biology , biochemistry , disease , microbiology and biotechnology
Excessive fructose intake is a risk factor for gut symptoms in patients with inflammatory bowel disease, however, its effect on the intestinal tract has not been evaluated previously. The present study investigated the impact of a high‑fructose diet (HFD) on intestinal barrier function in mice with experimental colitis. C57/BL6 mice were provided with either a HFD or control diet and either plain drinking water or water containing 1% dextran sulfate sodium (DSS) for 2 weeks. The disease activity index (DAI), pathological scores and expression of inflammatory cytokines were compared among the groups, and the proportions of fecal bacteria in the colon were analyzed. The body weight and colon length were significantly decreased, and the DAI and pathological scores were significantly increased in the DSS/HFD‑treated mice compared with the non‑DSS‑treated and control diet mice. Regarding the expression of inflammatory cytokines, the levels of interleukin (IL)‑6, IL‑1β and tumor necrosis factor‑α were significantly increased, and the expression of the tight junction protein occludin was significantly decreased in the DSS/HFD‑treated mice. The total bacterial count was increased in the HFD mice. Taken together, these results indicate that an HFD resulted in the deterioration of intestinal barrier function and increased susceptibility to DSS‑induced colitis.