Tier 3 — preclinical

Betaine supplementation alleviates dextran sulfate sodium-induced colitis via regulating the inflammatory response, enhancing the intestinal barrier, and altering gut microbiota

Nannan Zhao, Yuhang Yang, Chen Chen, Tengfang Jing, Yun Hu, Haixu Xu, Shuai Wang, Yu He, Enqi Liu, Jue Cui
Food & function 2022 13(24):12814-12826

Bibliography

PubMed
PMID 36422855
Funding
Funding was not specified in the indexed record or accessible funding metadata.
Competing interests
A competing-interest declaration was not available in the indexed record or accessible disclosure metadata.

Study snapshot

DesignExperimental animal and/or laboratory research
ModelDSS-treated mice and Caco-2 cells
SampleExperiment-specific biological replicates and model groups; see original methods
InterventionExperimental betaine exposure
DurationModel-specific colitis and cell protocols
EndpointsColitis; Intestinal barrier; Microbiota

What the study showed, in plain terms

Published in 2022, this source examined preclinical aging, brain and metabolic mechanisms. Design: Experimental animal and/or laboratory research. Sample/model: Experiment-specific biological replicates and model groups; see original methods. The exposure or intervention was Experimental betaine exposure. Follow-up or treatment period: Model-specific colitis and cell protocols.

Betaine improved selected inflammatory and barrier measures and altered the microbiome in the mouse model.

Experimental model evidence. The intervention, concentrations and outcomes do not establish an effective human supplement dose or a clinical treatment benefit.

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Key findings

  • Betaine improved selected inflammatory and barrier measures and altered the microbiome in the mouse model.
  • The recorded outcome domains were Colitis; Intestinal barrier; Microbiota.
  • The result applies to the tested exposure: Experimental betaine exposure; Model-specific colitis and cell protocols.

What this study can and cannot tell us

  • Experimental model evidence. The intervention, concentrations and outcomes do not establish an effective human supplement dose or a clinical treatment benefit.
  • Cell concentrations, species, disease models and experimental routes cannot be converted directly into an effective or safe oral human regimen.
  • Source basis: Indexed abstract and bibliographic data. Missing method details, funding information or participant denominators are not inferred.

Editorial review

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