Tier 4 — mechanistic

Variability of plasma and urine betaine in diabetes mellitus and its relationship to methionine load test responses: an observational study

Michael Lever, Sandy Slow, David O McGregor, Warwick J Dellow, Peter M George, Stephen T Chambers
Cardiovascular diabetology 2012 11:34

Bibliography

PubMed
PMID 22510294
PubMed Central
PMC3395555
DOI
10.1186/1475-2840-11-34
Funding
Funding was not specified in the indexed record or accessible funding metadata.
Competing interests
Reported disclosure: Competing interestsThere are no competing interests to declare.

Study snapshot

DesignObservational challenge study
ModelHuman participants
Sample34 adults with type 2 diabetes and 17 controls
InterventionMeasured betaine status and related metabolites; no randomized TMG treatment
DurationFasting and post-methionine testing
EndpointsDiabetes; Betaine variability; Homocysteine

What the study showed, in plain terms

Published in 2012, this source examined human observational and biomarker research. Design: Observational challenge study. Sample/model: 34 adults with type 2 diabetes and 17 controls. The exposure or intervention was Measured betaine status and related metabolites; no randomized TMG treatment. Follow-up or treatment period: Fasting and post-methionine testing.

Betaine levels and urinary losses were more variable in diabetes, and circulating betaine predicted post-load homocysteine responses.

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

Continue with TMG Data Center

Continue with TMG for Weight Loss: Body-Fat Findings and Their Limits

Key findings

  • Betaine levels and urinary losses were more variable in diabetes, and circulating betaine predicted post-load homocysteine responses.
  • The recorded outcome domains were Diabetes; Betaine variability; Homocysteine.
  • The exposure was observed rather than assigned as an isolated supplement treatment.

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.
  • Confounding, dietary patterns, illness, medication use and reverse causation can influence an association. Blood or dietary concentrations do not identify the effect of starting a capsule.
  • Source basis: Accessible full-text extract plus indexed bibliographic data. Missing method details, funding information or participant denominators are not inferred.

Related papers in the corpus

Tier 4
Dietary Choline and Betaine Are Not Associated With the Risk of Type 2 Diabetes. A Systematic Review and Meta-Analysis of Observational Studies
Elham Sharifi-Zahabi et al. · Journal of diabetes research · 2026
Tier 2
Metabolic Effects of Betaine: A Randomized Clinical Trial of Betaine Supplementation in Prediabetes
Ana Maria Grizales et al. · The Journal of clinical endocrinology and metabolism · 2018
Tier 4
High Betaine, a Trimethylamine N-Oxide Related Metabolite, Is Prospectively Associated with Low Future Risk of Type 2 Diabetes Mellitus in the PREVEND Study
Erwin Garcia et al. · Journal of clinical medicine · 2019
Tier 4
Associations between Serum Betaine, Methyl-Metabolizing Genetic Polymorphisms and Risk of Incident Type 2 Diabetes: A Prospective Cohort Study in Community-Dwelling Chinese Adults
Xiaoting Lu et al. · Nutrients · 2022
Tier 4
Dietary Choline and Betaine and Risk of CVD: A Systematic Review and Meta-Analysis of Prospective Studies
Katie A Meyer et al. · Nutrients · 2017
Tier 4
Association of choline and betaine with the risk of cardiovascular disease and all-cause mortality: Meta-analysis
Qinglin Yang et al. · European journal of clinical investigation · 2023

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