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Study · Animal study (in vivo) · mouse · 2018

1 result

Increased gut permeability in cancer cachexia: mechanisms and clinical relevance.

Bindels LB, Neyrinck AM, Loumaye A, Catry E, Walgrave H, Cherbuy C, Leclercq S, Van Hul M, Plovier H, Pachikian B, Bermúdez-Humarán LG, Langella P, Cani PD, Thissen JP, Delzenne NM

Oncotarget6 Apr 2018Cited by 130 (Europe PMC)

PMID29719601 (opens in a new tab)PMCIDPMC5915068 (opens in a new tab)DOI10.18632/oncotarget.24804 (opens in a new tab)PepBankPUB-29719601
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Summary

Intestinal disorders often occur in cancer patients, in association with body weight loss, and this alteration is commonly attributed to the chemotherapy. Here, using a mouse model of cancer cachexia induced by ectopic transplantation of C26 cancer cells, we discovered a profound alteration in the gut functions (gut permeability, epithelial turnover, gut immunity, microbial dysbiosis) independently of any chemotherapy. These alterations occurred independently of anorexia and were driven by interleukin 6. Gut dysfunction was found to be resistant to treatments with an anti-inflammatory bacterium (Faecalibacterium prausnitzii) or with gut peptides involved in intestinal cell renewal (teduglutide, a glucagon-like peptide 2 analogue). The translational value of our findings was evaluated in 152 colorectal and lung cancer patients with or without cachexia. The serum level of the lipopolysaccharide-binding protein, often presented as a reflection of the bacterial antigen load, was not only increased in cachectic mice and cancer patients, but also strongly correlated with the serum IL-6 level and predictive of death and cachexia occurrence in these patients. Altogether, our data highlight profound alterations of the intestinal homeostasis in cancer cachexia occurring independently of any chemotherapy and food intake reduction, with potential relevance in humans. In addition, we point out the lipopolysaccharide-binding protein as a new biomarker of cancer cachexia related to gut dysbiosis.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study1

1 result from studies that gave the peptide. No result from this study comes from people.

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In mice with C26 cancer cachexia, gut dysfunction resisted teduglutide treatment.

    In plain wordsIn mice with cancer cachexia, teduglutide did not resolve gut dysfunction.

    Peptide
    Teduglutide
    Outcome
    No significant changeGut dysfunction
    Study

    mousen: not reported in source

    C26 cancer cachexia
    Outcome group
    Gastrointestinal protection · Gastrointestinal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Gut dysfunction was found to be resistant to treatments with an anti-inflammatory bacterium (Faecalibacterium prausnitzii) or with gut peptides involved in intestinal cell renewal (teduglutide, a glucagon-like peptide 2 analogue).
    1 context sentence
    Summary · context
    Here, using a mouse model of cancer cachexia induced by ectopic transplantation of C26 cancer cells, we discovered a profound alteration in the gut functions (gut permeability, epithelial turnover, gut immunity, microbial dysbiosis) independently of any chemotherapy.

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Version history

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  1. Version 2Current

    28 Oct 2026, 02:03 UTC

    Study results updated

  2. Version 1

    27 Oct 2026, 16:37 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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