Evidence map›Paper›PMID 24586510›Full record

ArticlePloS one2014

The relationship between BCMO1 gene variants and macular pigment optical density in persons with and without age-related macular degeneration.

Beatrix Feigl, C Phillip Morris, Joanne Voisey, Anthony Kwan, Andrew J Zele

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.2field-weighted citation impact, top 24% 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

8 citing papers in PubMed, 15 citations in OpenAlex.

  1. Trial
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  4. Enzymology of vertebrate carotenoid oxygenases.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2020
    Review
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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

5 authors at 2 institutions in 1 country.

Beatrix FeiglInstitute of Health and Biomedical Innovation, Queensland University of Technology, Brisbane, QLD, Australia ; School of Biomedical Sciences, Queensland University of Technology, Brisbane, QLD, Australia ; Queensland Eye Institute, Brisbane, QLD, Australia.
C Phillip MorrisInstitute of Health and Biomedical Innovation, Queensland University of Technology, Brisbane, QLD, Australia ; School of Biomedical Sciences, Queensland University of Technology, Brisbane, QLD, Australia.
Joanne VoiseyInstitute of Health and Biomedical Innovation, Queensland University of Technology, Brisbane, QLD, Australia ; School of Biomedical Sciences, Queensland University of Technology, Brisbane, QLD, Australia.
Anthony KwanQueensland Eye Institute, Brisbane, QLD, Australia ; Faculty of Health Sciences, University of Queensland, Brisbane, QLD, Australia.
Andrew J ZeleInstitute of Health and Biomedical Innovation, Queensland University of Technology, Brisbane, QLD, Australia ; School of Optometry and Vision Sciences, Queensland University of Technology, Brisbane, QLD, Australia.
Queensland University of Technology · AUQueensland Eye Institute · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRecent evidence indicates that gene variants related to carotenoid metabolism play a role in the uptake of macular pigments lutein (L) and zeaxanthin (Z). Moreover, these pigments are proposed to reduce the risk for advanced age-related macular degeneration (AMD). This study provides the initial examination of the relationship between the gene variants related to carotenoid metabolism, macular pigment optical density (MPOD) and their combined expression in healthy humans and patients with AMD. PARTICIPANTS AND

methodsForty-four participants were enrolled from a general population and a private practice including 20 healthy participants and 24 patients with advanced (neovascular) AMD. Participants were genotyped for the three single nucleotide polymorphisms (SNPs) upstream from BCMO1, rs11645428, rs6420424 and rs6564851 that have been shown to either up or down regulate beta-carotene conversion efficiency in the plasma. MPOD was determined by heterochromatic flicker photometry.

resultsHealthy participants with the rs11645428 GG genotype, rs6420424 AA genotype and rs6564851 GG genotype all had on average significantly lower MPOD compared to those with the other genotypes (p<0.01 for all three comparisons). When combining BCMO1 genotypes reported to have "high" (rs11645428 AA/rs6420424 GG/rs6564851 TT) and "low" (rs11645428 GG/rs6420424 AA/rs6564851 GG) beta-carotene conversion efficiency, we demonstrate clear differences in MPOD values (p<0.01). In patients with AMD there were no significant differences in MPOD for any of the three BCMO1 gene variants.

conclusionIn healthy participants MPOD levels can be related to high and low beta-carotene conversion BCMO1 genotypes. Such relationships were not found in patients with advanced neovascular AMD, indicative of additional processes influencing carotenoid uptake, possibly related to other AMD susceptibility genes. Our findings indicate that specific BCMO1 SNPs should be determined when assessing the effects of carotenoid supplementation on macular pigment and that their expression may be influenced by retinal disease.

Indexed as

Polymorphism, Single Nucleotidebeta-Carotene 15,15'-MonooxygenaseCase-Control StudiesFemaleGene FrequencyGenetic LinkageGenetic Predisposition to DiseaseHumansMacular DegenerationMacular PigmentMaleMiddle AgedBCO1 protein, humanbeta-Carotene 15,15'-MonooxygenaseMacular Pigment

Identifiers

PMID24586510
PMCPMC3929644
OpenAlexW2071030457

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.