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Session: Nutritional Immunology and Inflammation (Poster Theater Flash Session 21)

(PTFS21-01-24) Partially Hydrolyzed Guar Gum Increases Susceptibility to Colitis and Colon Tumorigenesis in Mice

Tuesday, July 2, 2024
8:00 AM – 8:04 AM CT
Location:  W185A-C

    Presenting Author(s)

  • Sangshan Tian, MS (she/her/hers)

    Ph.D. candidate
    The Pennsylvania State University
    University Park, Pennsylvania, United States

    Disclosure(s): No relevant financial relationship(s) with ineligible companies to disclose.

    • Co-Author(s)

  • Rita Castro, PhD

    Research Assistant Professor
    The Pennsylvania State University
    University Park, Pennsylvania, United States

  • UG

    Umesh Kumar Goand, PhD

    Post Doctoral scholar
    The Pennsylvania State University
    State College, Pennsylvania, United States

  • GL

    Giang V. Le

    The Pennsylvania State University
    University Park, Pennsylvania, United States

  • DP

    Devendra Paudel, MS

    Graduate Research Assistant
    The Pennsylvania State University
    State College, Pennsylvania, United States

  • Vishal Singh, PhD

    Assistant Professor
    The Pennsylvania State University
    University Park, Pennsylvania, United States

Objectives: Partially hydrolyzed guar gum (PHGG) is a soluble fiber commonly promoted as a prebiotic to improve intestinal health. PHGG is derived from guar gum, which has been shown to have both beneficial and detrimental effects on colonic inflammation and tumorigenesis. These contrasting findings about guar gum's impact on intestinal health prompted us to investigate the effects of PHGG on colitis and colitis-associated colon carcinogenesis (CAC).

Methods: Four-week-old wild-type (WT) mice (C57BL/6) were maintained on an isocaloric diet containing either 7.5% PHGG and 2.5% cellulose (PHGG group) or 10% cellulose (control group) for 4 weeks. Subsequently, a subgroup of mice in each group (n= 6) was switched to drinking water supplemented with 1.4% dextran sulfate sodium (DSS) for 7 days to induce colitis. In another subgroup (n= 6), CAC was induced by a single injection of azoxymethane (AOM, 7.5 mg/kg b. wt.) followed by three 7-day cycles alternating between DSS and regular water. A diet with a lower amount of PHGG (2.5% PHGG and 7.5% cellulose) was used to assess the dose-dependent effect of PHGG on colitis and CAC development (n= 6).

Results: PHGG-fed mice developed more severe colitis than the control group after DSS administration. This phenotype was characterized by substantial bodyweight loss, elevated colonic inflammatory markers, disrupted crypt architecture, and extensive immune cell infiltration in the colon. Notably, PHGG feeding led to extensive colon tumorigenesis in the AOM/DSS model, whereas the control group displayed no visible tumors. The low-PHGG group also exhibited colitis and tumorigenesis, although the severity was markedly lower than in the PHGG group. These observations suggest a dose-dependent effect of PHGG on colitis and CAC development.

Conclusions: Our study demonstrates that PHGG exacerbated colitis and associated colon tumorigenesis, warranting further investigation into the potential gastrointestinal health risks associated with PHGG consumption.

Funding Sources: 1) Career Development Award [ID# 597229] from the Crohn’s & Colitis Foundation (CCF) to VS
2) This work was supported by NIH award R01DK133334-01A1