Evidence map›Paper›PMID 42614385›Full record

ArticleFrontiers in nutrition2026

Krill oil supplementation alleviates clinical symptoms and improves intestinal barrier function with transcriptomic associations to cell adhesion molecule pathways in a mouse model of spontaneous chronic colitis.

Yingying Liu, Ainsley M Robinson, Kulmira Nurgali, Xiao Qun Su

Abstract read
In one paragraph

Article in Frontiers in nutrition, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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3 · Its place in the literature

Who cites it

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No citing paper in PubMed yet.

4 · The record

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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Yingying LiuInstitute for Health & Sport, Victoria University, Melbourne, VIC, Australia.
Ainsley M RobinsonInstitute for Health & Sport, Victoria University, Melbourne, VIC, Australia.
Kulmira NurgaliInstitute for Health & Sport, Victoria University, Melbourne, VIC, Australia.
Xiao Qun SuInstitute for Health & Sport, Victoria University, Melbourne, VIC, Australia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Conventional therapies for inflammatory bowel disease (IBD) are associated with significant adverse effects, highlighting the need for safer and effective alternatives. Krill oil (KO), a rich source of long-chain omega-3 polyunsaturated fatty acids (PUFAs) and astaxanthin, has shown therapeutic potential in several disorders but remains understudied in chronic colitis. This study evaluates the potential therapeutic efficacy of KO, alone or in combination with dexamethasone (DEX), in a spontaneous chronic colitis mouse model that closely mimics human IBD. The molecular mechanisms underlying the health benefits of KO were also explored. Methods: Four groups of homozygous Results: Treatments with KO, DEX, and KO + DEX significantly reduced disease severity and mucosal injury. Restoration of colonic permeability was observed across all treatment groups, with KO + DEX and DEX treatments notably enhancing the expression of tight junction proteins. Transcriptomic profiling identified changes in epithelial barrier-related and cell adhesion molecules (CAM)-related genes following KO treatment, including higher expression of Conclusion: KO treatment showed promising therapeutic benefits, with some being comparable to DEX, and enhanced efficacy when combined with DEX, in a mouse model of spontaneous chronic colitis by restoring epithelial barrier integrity and suppressing CAM-mediated immune cell recruitment.

Indexed as

cell adhesion molecule (CAM) pathwayscolonic permeabilitydexamethasoneIBDkrill oilWinnie mice

Identifiers

PMID42614385
PMCPMC13481495

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.