Tier 3 — preclinical

Betaine modulates age-related NF-kappaB by thiol-enhancing action

Eun Kyung Go, Kyung Jin Jung, Ji Min Kim, Hyunae Lim, Hyeang Kwan Lim, Byung Pal Yu, Hae Young Chung
Biological & pharmaceutical bulletin 2007 30(12):2244-2249

Bibliography

PubMed
PMID 18057706
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
ModelAged rats and HEK293T cells
SampleExperiment-specific biological replicates and model groups; see original methods
InterventionDietary betaine and glutathione-depletion cell challenges
Duration10-day rat feeding experiment
EndpointsThiol status; NF-kappaB; Aging mechanisms

What the study showed, in plain terms

Published in 2007, 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 Dietary betaine and glutathione-depletion cell challenges. Follow-up or treatment period: 10-day rat feeding experiment.

Betaine modified thiol status and reduced selected NF-kappaB-related inflammatory signals in the experimental systems.

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 modified thiol status and reduced selected NF-kappaB-related inflammatory signals in the experimental systems.
  • The recorded outcome domains were Thiol status; NF-kappaB; Aging mechanisms.
  • The result applies to the tested exposure: Dietary betaine and glutathione-depletion cell challenges; 10-day rat feeding experiment.

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.

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