Tier 3 — preclinical

Effect of betaine on hepatic insulin resistance through FOXO1-induced NLRP3 inflammasome

Dae Hyun Kim, Seong Min Kim, Bonggi Lee, Eun Kyeong Lee, Ki Wung Chung, Kyoung Mi Moon, Hye Jin An, Kyung Mok Kim, Byung Pal Yu, Hae Young Chung
The Journal of nutritional biochemistry 2017 45:104-114

Bibliography

PubMed
PMID 28499186
DOI
10.1016/j.jnutbio.2017.04.014
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
ModelDiabetic mice and HepG2 cells
SampleExperiment-specific biological replicates and model groups; see original methods
InterventionMouse betaine 50 mg/kg/day plus cell experiments
Duration3 weeks in mice
EndpointsInsulin signaling; NLRP3 inflammasome; Oxidative stress

What the study showed, in plain terms

Published in 2017, 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 Mouse betaine 50 mg/kg/day plus cell experiments. Follow-up or treatment period: 3 weeks in mice.

Inflammasome and oxidative-stress signals were reduced, with evidence involving FOXO1 and TXNIP interactions.

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

  • Inflammasome and oxidative-stress signals were reduced, with evidence involving FOXO1 and TXNIP interactions.
  • The recorded outcome domains were Insulin signaling; NLRP3 inflammasome; Oxidative stress.
  • The result applies to the tested exposure: Mouse betaine 50 mg/kg/day plus cell experiments; 3 weeks in mice.

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