Evidence map›Paper›PMID 32481712›Full record

ReviewInternational journal of molecular sciences2020

Riboflavin Deficiency-Implications for General Human Health and Inborn Errors of Metabolism.

Signe Mosegaard, Graziana Dipace, Peter Bross, Jasper Carlsen, Niels Gregersen, Rikke Katrine Jentoft Olsen

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers.

0numbers the graph read from it
0cells of the map it votes in
94citing papers in PubMed
12.2field-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

94 citing papers in PubMed, 196 citations in OpenAlex.

  1. Assessment of vitamin A, vitamin BEuropean journal of nutrition · 2025
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34 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

6 authors at 1 institution in 2 countries.

Signe MosegaardResearch Unit for Molecular Medicine, Department for Clinical Medicine, Aarhus University and Aarhus University Hospital, 8200 Aarhus N, Denmark.
Graziana DipaceResearch Unit for Molecular Medicine, Department for Clinical Medicine, Aarhus University and Aarhus University Hospital, 8200 Aarhus N, Denmark.ORCID 0000-0003-0963-2744
Peter BrossResearch Unit for Molecular Medicine, Department for Clinical Medicine, Aarhus University and Aarhus University Hospital, 8200 Aarhus N, Denmark.ORCID 0000-0001-9526-8525
Jasper CarlsenResearch Unit for Molecular Medicine, Department for Clinical Medicine, Aarhus University and Aarhus University Hospital, 8200 Aarhus N, Denmark.
Niels GregersenResearch Unit for Molecular Medicine, Department for Clinical Medicine, Aarhus University and Aarhus University Hospital, 8200 Aarhus N, Denmark.
Rikke Katrine Jentoft OlsenResearch Unit for Molecular Medicine, Department for Clinical Medicine, Aarhus University and Aarhus University Hospital, 8200 Aarhus N, Denmark.
Aarhus University Hospital · DK

Funding

Lundbeckfonden R263-2017-4384
6 · The paper itself

Abstract

As an essential vitamin, the role of riboflavin in human diet and health is increasingly being highlighted. Insufficient dietary intake of riboflavin is often reported in nutritional surveys and population studies, even in non-developing countries with abundant sources of riboflavin-rich dietary products. A latent subclinical riboflavin deficiency can result in a significant clinical phenotype when combined with inborn genetic disturbances or environmental and physiological factors like infections, exercise, diet, aging and pregnancy. Riboflavin, and more importantly its derivatives, flavin mononucleotide (FMN) and flavin adenine dinucleotide (FAD), play a crucial role in essential cellular processes including mitochondrial energy metabolism, stress responses, vitamin and cofactor biogenesis, where they function as cofactors to ensure the catalytic activity and folding/stability of flavoenzymes. Numerous inborn errors of flavin metabolism and flavoenzyme function have been described, and supplementation with riboflavin has in many cases been shown to be lifesaving or to mitigate symptoms. This review discusses the environmental, physiological and genetic factors that affect cellular riboflavin status. We describe the crucial role of riboflavin for general human health, and the clear benefits of riboflavin treatment in patients with inborn errors of metabolism.

Indexed as

MutationAcyl-CoA DehydrogenasesAgingAnimalsDietElectron TransportEnergy MetabolismFatty AcidsFemaleFlavin-Adenine DinucleotideFlavin MononucleotideFolic AcidGenetic VariationHomocysteineHumansImmune SystemAcyl-CoA DehydrogenasesFatty AcidsFlavin-Adenine DinucleotideFlavin MononucleotideFolic AcidHomocysteineRiboflavinacyl-CoA dehydrogenaseselectron transport chainenergy metabolismfatty acid oxidationfoldinginborn errors of metabolismMADDmitochondriariboflavinriboflavin deficiency

Identifiers

PMID32481712
PMCPMC7312377
OpenAlexW3031970934

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.