Tier 3 — preclinical

Long-term betaine therapy in a murine model of cystathionine beta-synthase deficient homocystinuria: decreased efficacy over time reveals a significant threshold effect between elevated homocysteine and thrombotic risk

Kenneth N Maclean, Hua Jiang, Lori S Greiner, Robert H Allen, Sally P Stabler
Molecular genetics and metabolism 2012 105(3):395-403

Bibliography

PubMed
PMID 22192524
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
ModelCBS-deficient mice
SampleExperiment-specific biological replicates and model groups; see original methods
InterventionProlonged betaine treatment without methionine restriction
DurationLong-term experimental treatment
EndpointsTreatment durability; BHMT; Thrombotic phenotype

What the study showed, in plain terms

Published in 2012, 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 Prolonged betaine treatment without methionine restriction. Follow-up or treatment period: Long-term experimental treatment.

Homocysteine-lowering efficacy diminished over time and inflammatory/coagulation abnormalities returned as homocysteine rose.

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

  • Homocysteine-lowering efficacy diminished over time and inflammatory/coagulation abnormalities returned as homocysteine rose.
  • The recorded outcome domains were Treatment durability; BHMT; Thrombotic phenotype.
  • The result applies to the tested exposure: Prolonged betaine treatment without methionine restriction; Long-term experimental treatment.

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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