Tier 4 — mechanistic

Assessment of urinary betaine as a marker of diabetes mellitus in cardiovascular patients

Hall Schartum-Hansen, Per M Ueland, Eva R Pedersen, Klaus Meyer, Marta Ebbing, Øyvind Bleie, Gard F T Svingen, Reinhard Seifert, Bjørn E Vikse, Ottar Nygård
PloS one 2013 8(8):e69454

Bibliography

PubMed
PMID 23936331
PubMed Central
PMC3735559
DOI
10.1371/journal.pone.0069454
Funding
Reported funding/support: This work was funded by the University of Bergen, Bergen, Norway, the Nordic Centre of Excellence Programme on Food, Nutrition and Health - MitoHealth, Bergen, Norway and the Foundation to Promote Research into Functional Vitamin B12-Deficiency, Bergen, Norway. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Competing interests
Reported disclosure: Competing Interests: The authors have declared that no competing interests exist.

Study snapshot

DesignProspective patient biomarker analysis
ModelHuman participants
Sample2396 coronary-evaluation patients in WENBIT
InterventionMeasured betaine status and related metabolites; no randomized TMG treatment
DurationMedian 39 months
EndpointsUrinary betaine; Diabetes prediction

What the study showed, in plain terms

Published in 2013, this source examined human observational and biomarker research. It examined Measured betaine status and related metabolites; no randomized TMG treatment. The source describes 2396 coronary-evaluation patients in WENBIT.

Greater urinary betaine loss was associated with existing diabetes and subsequent diabetes development.

Observational exposure analysis: residual confounding and reverse causation remain possible. Associations do not establish that betaine supplementation causes the same outcome.

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Key findings

  • Greater urinary betaine loss was associated with existing diabetes and subsequent diabetes development.
  • The recorded outcome domains were Urinary betaine; Diabetes prediction.

What this study can and cannot tell us

  • Observational exposure analysis: residual confounding and reverse causation remain possible. Associations do not establish that betaine supplementation causes the same outcome.
  • Source basis: Accessible full-text extract plus indexed bibliographic data. Missing method details, funding information or participant denominators are not inferred.

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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