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    Manipulation of the gut microbiota using resistant starch is associated with protection against colitis-associated colorectal cancer in rats

    Access Status
    Fulltext not available
    Authors
    Hu, Y.
    Le Leu, R.
    Christophersen, Claus
    Somashekar, R.
    Conlon, M.
    Meng, X.
    Winter, J.
    Woodman, R.
    McKinnon, R.
    Young, G.
    Date
    2015
    Type
    Journal Article
    
    Metadata
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    Citation
    Hu, Y. and Le Leu, R. and Christophersen, C. and Somashekar, R. and Conlon, M. and Meng, X. and Winter, J. et al. 2015. Manipulation of the gut microbiota using resistant starch is associated with protection against colitis-associated colorectal cancer in rats. Carcinogenesis. 37 (4): pp. 366-375.
    Source Title
    Carcinogenesis
    DOI
    10.1093/carcin/bgw019
    ISSN
    0143-3334
    School
    School of Molecular and Life Sciences (MLS)
    URI
    http://hdl.handle.net/20.500.11937/71266
    Collection
    • Curtin Research Publications
    Abstract

    © The Author 2016. Published by Oxford University Press. All rights reserved. This study evaluated whether dietary resistant starch (RS) and green tea extract (GTE), which have anti-inflammatory and anticancer properties, protect against colitis-associated colorectal cancer (CAC) using a rat model, also investigated potential mechanisms of action of these agents including their effects on the gut microbiota. Rats were fed a control diet or diets containing 10% RS, 0.5% GTE or a combination of the two (RS + GTE). CAC was initiated with 2 weekly azoxymethane (AOM) injections (10 mg/kg) followed by 2% dextran sodium sulphate in drinking water for 7 days after 2 weeks on diets. Rats were killed 20 weeks after the first AOM. Colon tissues and tumours were examined for histopathology by H&E, gene/protein expression by PCR and immunohistochemistry and digesta for analyses of fermentation products and microbiota populations. RS and RS + GTE (but not GTE) diets significantly (P < 0.05) decreased tumour multiplicity and adenocarcinoma formation, relative to the control diet. Effects of RS + GTE were not different from RS alone. RS diet caused significant shifts in microbial composition/diversity, with increases in Parabacteroides, Barnesiella, Ruminococcus, Marvinbryantia and Bifidobacterium as primary contributors to the shift. RS-containing diets increased short chain fatty acids (SCFA) and expression of the SCFA receptor GPR43 mRNA, and reduced inflammation (COX-2, NF-kB, TNF-a and IL-1ß mRNA) and cell proliferation P < 0.05. GTE had no effect. This is the first study that demonstrates chemopreventive effects of RS (but not GTE) in a rodent CAC model, suggesting RS might have benefit to patients with ulcerative colitis who are at an increased risk of developing CRC.

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