Tier 3 — preclinical

Betaine postpones hyperglycemia-related senescence in ovarian and testicular cells: Involvement of RAGE and β-galactosidase

Neda Mohammadi, Mina Hemmati, Behrouz Motlagh, Arezou Biyabani
Cell biochemistry and function 2024 42(2):e3973

Bibliography

PubMed
PMID 38488483
Funding
Indexed grant support: Zanjan University of Medical Sciences. 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
ModelCultured ovarian and testicular cells
SampleExperiment-specific biological replicates and model groups; see original methods
InterventionBetaine 5 mmol/L under high-glucose conditions
DurationIn vitro exposure
EndpointsCellular senescence; Oxidative stress

What the study showed, in plain terms

Published in 2024, 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 5 mmol/L under high-glucose conditions. Follow-up or treatment period: In vitro exposure.

Betaine reduced selected oxidative and senescence-associated markers in high-glucose cell cultures.

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 reduced selected oxidative and senescence-associated markers in high-glucose cell cultures.
  • The recorded outcome domains were Cellular senescence; Oxidative stress.
  • The result applies to the tested exposure: Betaine 5 mmol/L under high-glucose conditions; In vitro exposure.

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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