Tier 3 — preclinical

Urolithin A-mediated augmentation of intestinal barrier function through elevated secretory mucin synthesis

Yasuda T, Takagi T, Asaeda K, Hashimoto H, Kajiwara M, Azuma Y, Kitae H, Hirai Y, Mizushima K, Doi T, Inoue K, Dohi O, Yoshida N, Uchiyama K, Ishikawa T, Konishi H, Ukawa Y, Kohara A, Kudoh M, Inoue R, Naito Y, Itoh Y
Scientific Reports 2024 14(1):15706

Bibliography

PubMed
PMID 38977770
PubMed Central
PMC11231190
DOI
10.1038/s41598-024-65791-x
Funding
Daicel Corporation partly supported the work.

Study snapshot

DesignMouse mechanistic study with Nrf2-deficient and AHR-antagonist experiments plus mucin-producing cell assays
ModelWild-type and Nrf2-deficient mice, DSS colitis model and LS174T mucin-producing cells
SampleMultiple animal and cellular experimental cohorts
InterventionUrolithin A treatment
DurationVaried by experiment
EndpointsMUC2 expression and mucus thickness; Gut permeability; DSS colitis; Nrf2 and AHR signaling; Short-chain-fatty-acid-producing bacteria

What the study showed, in plain terms

This 2024 study found that Urolithin A increased colonic mucus production through Nrf2 and AHR signaling, reduced gut permeability and improved experimental colitis in mice. It provides a second independent mechanistic line for gut-barrier content, but not human clinical proof.

Key findings

Colonic mucus thickness and MUC2 expression increased.

Gut permeability fell in mouse experiments.

DSS colitis severity improved.

Nrf2 and AHR signaling were required for key barrier effects.

What this study can and cannot tell us

No human supplementation outcomes were tested.

Cell and mouse barrier effects may not translate quantitatively to people.

The work received partial corporate funding from Daicel.

Editorial review

Reviewed by the Biohack Blueprint research team

Last verified

Dr. Khaled Mahmoud, MBBChCritical Care Medicine, Longevity Science & Editorial Direction Dr. Amr Yasser, PhDCardiometabolic, Musculoskeletal, Gut & Bioavailability Dr. Abdulla Mostafa, PhDCellular Senescence, Neurological, Mitochondrial & Brain-Ageing Biology