Evidence map›Paper›PMID 24022817›Full record

ReviewNutrients2013

The metabolic burden of methyl donor deficiency with focus on the betaine homocysteine methyltransferase pathway.

Rima Obeid

Open access · goldAbstract readReview
In one paragraph

Review in Nutrients, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 137 papers.

0numbers the graph read from it
0cells of the map it votes in
137citing papers in PubMed
12.1field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

137 citing papers in PubMed, 274 citations in OpenAlex.

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  15. Betaine Alters the Interplay of the Adenosine andInternational journal of molecular sciences · 2026
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  20. Review

77 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Rima ObeidDepartment of Clinical Chemistry, University Hospital of the Saarland, D-66424, Homburg, Germany. rima.obeid@uniklinikum-saarland.de.
Saarland University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Methyl groups are important for numerous cellular functions such as DNA methylation, phosphatidylcholine synthesis, and protein synthesis. The methyl group can directly be delivered by dietary methyl donors, including methionine, folate, betaine, and choline. The liver and the muscles appear to be the major organs for methyl group metabolism. Choline can be synthesized from phosphatidylcholine via the cytidine-diphosphate (CDP) pathway. Low dietary choline loweres methionine formation and causes a marked increase in S-adenosylmethionine utilization in the liver. The link between choline, betaine, and energy metabolism in humans indicates novel functions for these nutrients. This function appears to goes beyond the role of the nutrients in gene methylation and epigenetic control. Studies that simulated methyl-deficient diets reported disturbances in energy metabolism and protein synthesis in the liver, fatty liver, or muscle disorders. Changes in plasma concentrations of total homocysteine (tHcy) reflect one aspect of the metabolic consequences of methyl group deficiency or nutrient supplementations. Folic acid supplementation spares betaine as a methyl donor. Betaine is a significant determinant of plasma tHcy, particularly in case of folate deficiency, methionine load, or alcohol consumption. Betaine supplementation has a lowering effect on post-methionine load tHcy. Hypomethylation and tHcy elevation can be attenuated when choline or betaine is available.

Indexed as

Metabolic Networks and PathwaysAnimalsBetaineBetaine-Homocysteine S-MethyltransferaseCholineDietary SupplementsDisease Models, AnimalDNA MethylationFastingFatty LiverFolic AcidHomocysteineHumansLiverMethionineMuscular DiseasesBetaineBetaine-Homocysteine S-MethyltransferaseCholineFolic AcidHomocysteineMethionineS-Adenosylmethionine

Identifiers

PMID24022817
PMCPMC3798916
OpenAlexW2090630252

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.