Tier 3 — preclinical

Betaine supplementation prevents fatty liver induced by a high-fat diet: effects on one-carbon metabolism

Rafael Deminice, Robin P da Silva, Simon G Lamarre, Karen B Kelly, René L Jacobs, Margaret E Brosnan, John T Brosnan
Amino acids 2015 47(4):839-846

Bibliography

PubMed
PMID 25577261
Funding
Indexed grant support: Canadian Institutes of Health Research — Canada. The indexed list may not contain the complete funding declaration.
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
ModelHigh-fat-fed rats
SampleExperiment-specific biological replicates and model groups; see original methods
InterventionBetaine added to the experimental diet
Duration3 weeks
EndpointsLiver fat; One-carbon metabolism

What the study showed, in plain terms

Published in 2015, 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 Betaine added to the experimental diet. Follow-up or treatment period: 3 weeks.

Betaine reduced diet-induced liver-fat accumulation and altered SAM-related one-carbon metabolism in rats.

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 reduced diet-induced liver-fat accumulation and altered SAM-related one-carbon metabolism in rats.
  • The recorded outcome domains were Liver fat; One-carbon metabolism.
  • The result applies to the tested exposure: Betaine added to the experimental diet; 3 weeks.

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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