Evidence map›Paper›PMID 27383215›Full record

ArticlePloS one2016

Type 2 Diabetes Risk Allele Loci in the Qatari Population.

Sarah L O'Beirne, Jacqueline Salit, Juan L Rodriguez-Flores, Michelle R Staudt, Charbel Abi Khalil, Khalid A Fakhro, Amal Robay, Monica D Ramstetter, Iman K Al-Azwani, Joel A Malek and 13 more

Erratum issuedAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 20 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 3 pooled it
–field-weighted citation impact
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

20 citing papers in PubMed, 3 syntheses or guidelines pooled it.

  1. Pooled it
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  11. Vitamin DBMC endocrine disorders · 2020
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  14. Association of Differing Qatari Genotypes with Vitamin D Metabolites.International journal of endocrinology · 2020
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

23 authors.

Sarah L O'BeirneDepartment of Genetic Medicine, Weill Cornell Medical College, New York, New York, United States of America.
Jacqueline SalitDepartment of Genetic Medicine, Weill Cornell Medical College, New York, New York, United States of America.
Juan L Rodriguez-FloresDepartment of Genetic Medicine, Weill Cornell Medical College, New York, New York, United States of America.
Michelle R StaudtDepartment of Genetic Medicine, Weill Cornell Medical College, New York, New York, United States of America.
Charbel Abi KhalilDepartment of Genetic Medicine, Weill Cornell Medical College-Qatar, Doha, Qatar.
Khalid A FakhroDepartment of Genetic Medicine, Weill Cornell Medical College-Qatar, Doha, Qatar.
Amal RobayDepartment of Genetic Medicine, Weill Cornell Medical College-Qatar, Doha, Qatar.
Monica D RamstetterDepartment of Genetic Medicine, Weill Cornell Medical College, New York, New York, United States of America.
Iman K Al-AzwaniDepartment of Genetic Medicine, Weill Cornell Medical College-Qatar, Doha, Qatar.
Joel A MalekDepartment of Genetic Medicine, Weill Cornell Medical College-Qatar, Doha, Qatar.
Mahmoud ZirieDepartment of Medicine, Hamad Medical Corporation, Doha, Qatar.
Amin JayyousiDepartment of Medicine, Hamad Medical Corporation, Doha, Qatar.
Ramin BadiiLaboratory Medicine and Pathology, Hamad Medical Corporation, Doha, Qatar.
Ajayeb Al-Nabet Al-MarriLaboratory Medicine and Pathology, Hamad Medical Corporation, Doha, Qatar.
Maria J ChiuchioloDepartment of Genetic Medicine, Weill Cornell Medical College, New York, New York, United States of America.
Alya Al-ShakakiDepartment of Genetic Medicine, Weill Cornell Medical College-Qatar, Doha, Qatar.
Omar ChidiacDepartment of Genetic Medicine, Weill Cornell Medical College-Qatar, Doha, Qatar.
Maey GharbiahDepartment of Genetic Medicine, Weill Cornell Medical College-Qatar, Doha, Qatar.
Abdulbari BenerDepartment of Medical Statistics and Epidemiology, Hamad Medical Corporation, Doha, Qatar.
Dora StadlerDepartment of Medicine, Weill Cornell Medical College-Qatar, Doha, Qatar.
Neil R HackettDepartment of Genetic Medicine, Weill Cornell Medical College, New York, New York, United States of America.
Jason G MezeyDepartment of Genetic Medicine, Weill Cornell Medical College, New York, New York, United States of America.
Ronald G CrystalDepartment of Genetic Medicine, Weill Cornell Medical College, New York, New York, United States of America.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe prevalence of type 2 diabetes (T2D) is increasing in the Middle East. However, the genetic risk factors for T2D in the Middle Eastern populations are not known, as the majority of studies of genetic risk for T2D are in Europeans and Asians.

methodsAll subjects were ≥3 generation Qataris. Cases with T2D (n = 1,124) and controls (n = 590) were randomly recruited and assigned to the 3 known Qatari genetic subpopulations [Bedouin (Q1), Persian/South Asian (Q2) and African (Q3)]. Subjects underwent genotyping for 37 single nucleotide polymorphisms (SNPs) in 29 genes known to be associated with T2D in Europeans and/or Asian populations, and an additional 27 tag SNPs related to these susceptibility loci. Pre-study power analysis suggested that with the known incidence of T2D in adult Qataris (22%), the study population size would be sufficient to detect significant differences if the SNPs were risk factors among Qataris, assuming that the odds ratio (OR) for T2D SNPs in Qatari's is greater than or equal to the SNP with highest known OR in other populations.

resultsHaplotype analysis demonstrated that Qatari haplotypes in the region of known T2D risk alleles in Q1 and Q2 genetic subpopulations were similar to European haplotypes. After Benjamini-Hochberg adjustment for multiple testing, only two SNPs (rs7903146 and rs4506565), both associated with transcription factor 7-like 2 (TCF7L2), achieved statistical significance in the whole study population. When T2D subjects and control subjects were assigned to the known 3 Qatari subpopulations, and analyzed individually and with the Q1 and Q2 genetic subpopulations combined, one of these SNPs (rs4506565) was also significant in the admixed group. No other SNPs associated with T2D in all Qataris or individual genetic subpopulations.

conclusionsWith the caveats of the power analysis, the European/Asian T2D SNPs do not contribute significantly to the high prevalence of T2D in the Qatari population, suggesting that the genetic risks for T2D are likely different in Qataris compared to Europeans and Asians.

Indexed as

Polymorphism, Single NucleotideAdultAgedAllelesAsian PeopleCase-Control StudiesDiabetes Mellitus, Type 2Gene FrequencyGenomeGenotypeHaplotypesHumansIncidenceMaleMiddle AgedQatar

Identifiers

PMID27383215
PMCPMC4934876

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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.