Tier 3 — preclinical

Rectification of impaired adipose tissue methylation status and lipolytic response contributes to hepatoprotective effect of betaine in a mouse model of alcoholic liver disease

Xiaobing Dou, Yongliang Xia, Jing Chen, Ying Qian, Songtao Li, Ximei Zhang, Zhenyuan Song
British journal of pharmacology 2014 171(17):4073-4086

Bibliography

PubMed
PMID 24819676
PubMed Central
PMC4243980
DOI
10.1111/bph.12765
Funding
Indexed grant support: R01 AA017442 — NIAAA NIH HHS — United States. 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
ModelAlcohol-fed mice and adipocyte experiments
SampleExperiment-specific biological replicates and model groups; see original methods
InterventionBetaine 0.5% in the liquid diet
Duration5 weeks
EndpointsAdipose methylation; Lipolysis; Liver injury

What the study showed, in plain terms

Published in 2014, 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 0.5% in the liquid diet. Follow-up or treatment period: 5 weeks.

Betaine improved selected liver and adipose-tissue changes, including methylation-associated regulation of lipolysis.

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 liver and adipose-tissue changes, including methylation-associated regulation of lipolysis.
  • The recorded outcome domains were Adipose methylation; Lipolysis; Liver injury.
  • The result applies to the tested exposure: Betaine 0.5% in the liquid diet; 5 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.

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Editorial review

Reviewed by the Biohack Blueprint research team

Last verified

Dr. Khaled Mahmoud, MBBChCritical Care Medicine, Longevity Science & Editorial Direction Dr. Amr Yasser, PhDCardiometabolic, Musculoskeletal, Gut & Bioavailability Dr. Abdulla Mostafa, PhDCellular Senescence, Neurological, Mitochondrial & Brain-Ageing Biology