Tier 3 — preclinical

Involvement of AMP-activated protein kinase in beneficial effects of betaine on high-sucrose diet-induced hepatic steatosis

Zhenyuan Song, Ion Deaciuc, Zhanxiang Zhou, Ming Song, Theresa Chen, Daniell Hill, Craig J McClain
American journal of physiology. Gastrointestinal and liver physiology 2007 293(4):G894-G902

Bibliography

PubMed
PMID 17702954
PubMed Central
PMC4215798
Funding
Indexed grant support: R01 AA010496 — NIAAA NIH HHS — United States; R01 AA015970 — 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
ModelHigh-sucrose-fed mice
Sample32 mice; four groups of eight
InterventionBetaine 1% in drinking water
DurationLong-term dietary model
EndpointsLiver fat; AMPK; Lipogenesis

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: 32 mice; four groups of eight. The exposure or intervention was Betaine 1% in drinking water. Follow-up or treatment period: Long-term dietary model.

Betaine attenuated liver-fat accumulation alongside increased AMPK activation and reduced lipogenic activity.

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 attenuated liver-fat accumulation alongside increased AMPK activation and reduced lipogenic activity.
  • The recorded outcome domains were Liver fat; AMPK; Lipogenesis.
  • The result applies to the tested exposure: Betaine 1% in drinking water; Long-term dietary model.

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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