Evidence map›Paper›PMID 42654240›Full record

ArticleNutrients2026

Sucralose Alters Gut Microbiota, Intestinal Metabolites, and Epithelial Serotonergic Responses to Visceral Stimulation in Mice Exposed to Chronic Restraint Stress.

Akira Aoki, Jonathan P Jacobs, Yoshinori Okamoto

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In one paragraph

Article in Nutrients, 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

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0 citing papers in PubMed.

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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

3 authors.

Akira AokiFaculty of Pharmacy, Meijo University, 150 Yagotoyama, Tempaku-ku, Nagoya 468-8503, Japan.ORCID 0000-0002-2504-2894
Jonathan P JacobsVatche and Tamar Manoukian Division of Digestive Diseases, Department of Medicine, University of California, Los Angeles, CA 90095, USA.ORCID 0000-0003-4698-0254
Yoshinori OkamotoFaculty of Pharmacy, Meijo University, 150 Yagotoyama, Tempaku-ku, Nagoya 468-8503, Japan.ORCID 0000-0001-6031-3250

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

objectivesDietary modifiers of the gut ecosystem may influence intestinal and host responses associated with psychological stress. However, it remains unclear whether sucralose, a widely consumed non-nutritive sweetener, alters host-microbiota interactions following chronic stress exposure. We investigated the effects of short-term experimental sucralose exposure in mice previously subjected to chronic restraint stress (CRS).

methodsFollowing completion of the CRS protocol, mice received 0.03% or 0.1% sucralose in drinking water for 12 days. Intestinal phenotypes, cecal microbial community structure, microbial metabolites, colonic epithelial gene expression, and epithelial serotonergic responses following allyl isothiocyanate (AITC)-induced visceral stimulation were evaluated.

resultsColon length was significantly reduced in the 0.1% sucralose group, whereas intestinal permeability remained unchanged. Sucralose selectively altered colonic epithelial gene expression and was associated with changes in cecal microbial community structure without marked changes in alpha diversity. The relative abundance of Bacteroides acidifaciens was significantly reduced, particularly in the 0.1% sucralose group. Fecal acetate and cecal tryptophan concentrations were decreased following sucralose exposure. Following AITC-induced visceral stimulation, the CRS + 0.1% sucralose group exhibited reduced immobility behavior together with increased epithelial serotonin and 5-hydroxyindoleacetic acid concentrations.

conclusionsIn mice previously exposed to CRS, short-term sucralose exposure was associated with colon shortening, differences in cecal microbial community structure, reduced Bacteroides acidifaciens abundance, decreased fecal acetate and cecal tryptophan concentrations, and altered epithelial serotonergic responsiveness following visceral stimulation. The behavioral and epithelial serotonergic findings suggest that prior stress exposure may influence selected host responses to sucralose. These findings provide a basis for future studies examining how dietary sweeteners modify host-microbiota interactions following chronic stress exposure.

Indexed as

Gastrointestinal MicrobiomeIntestinal MucosaSerotoninStress, PsychologicalSucroseAnimalsCecumColonIsothiocyanatesMaleMiceMice, Inbred C57BLRestraint, Physicalallyl isothiocyanateIsothiocyanatesSerotoninSucrosetrichlorosucrosechronic restraint stressdisorders of gut–brain interactionhost–microbiota interactionsserotoninsucralosetryptophan metabolism

Identifiers

PMID42654240
PMCPMC13516141

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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.