Tier 3 — preclinical

Glycine betaine excretion is not directly linked to plasma glucose concentrations in hyperglycaemia

W J Dellow, S T Chambers, G K Barrell, M Lever, R A Robson
Diabetes research and clinical practice 2001 52(3):165-169

Bibliography

PubMed
PMID 11323085
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
ModelNonpregnant female sheep
SampleExperiment-specific biological replicates and model groups; see original methods
InterventionIntravenous glucose challenges; urinary betaine measured, not supplemented
Duration6-hour glucose infusion and 12-hour saline washout
EndpointsUrinary betaine; Glucose physiology

What the study showed, in plain terms

Published in 2001, 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 Intravenous glucose challenges; urinary betaine measured, not supplemented. Follow-up or treatment period: 6-hour glucose infusion and 12-hour saline washout.

Acute hyperglycemia did not directly raise betaine excretion in this animal experiment.

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

  • Acute hyperglycemia did not directly raise betaine excretion in this animal experiment.
  • The recorded outcome domains were Urinary betaine; Glucose physiology.
  • The result applies to the tested exposure: Intravenous glucose challenges; urinary betaine measured, not supplemented; 6-hour glucose infusion and 12-hour saline washout.

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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