Evidence map›Paper›PMID 30021629›Full record

Observational studyLipids in health and disease2018

Use of a gene score of multiple low-modest effect size variants can predict the risk of obesity better than the individual SNPs.

Shabana, Saleem Ullah Shahid, Shahida Hasnain

Open access · goldAbstract readObservational Study
In one paragraph

Observational study in Lipids in health and disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 21% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

  1. Pooled it
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  10. Antioxidants-Related Superoxide Dismutase (Antioxidants (Basel, Switzerland) · 2021
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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

3 authors at 1 institution in 1 country.

ShabanaDepartment of Microbiology and Molecular Genetics, University of the Punjab, Lahore, Pakistan. shabana.mmg@pu.edu.pk.ORCID http://orcid.org/0000-0002-6617-1588
Saleem Ullah ShahidDepartment of Microbiology and Molecular Genetics, University of the Punjab, Lahore, Pakistan.
Shahida HasnainDepartment of Microbiology and Molecular Genetics, University of the Punjab, Lahore, Pakistan.
University of the Punjab · PK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundObesity is a complex disorder, the development of which is modulated by a multitude of environmental, behavioral and genetic factors. The common forms of obesity are polygenic in nature which means that many variants in the same or different genes act synergistically and affect the body weight quantitatively. The aim of the current study was to use information from many common variants previously identified to affect body weight to construct a gene score and observe whether it improves the associations observed. The SNPs selected were G2548A in leptin (LEP) gene, Gln223Arg in leptin receptor (LEPR) gene, Ala54Thr in fatty acid binding protein 2 (FABP2) gene, rs1121980 in fat mass and obesity associated (FTO) gene, rs3923113 in Growth Factor Receptor Bound Protein 14 (GRB14), rs16861329 in Beta-galactoside alpha-2,6-sialyltransferase 1 (ST6GAL1), rs1802295 in Vacuolar protein sorting-associated protein 26A (VPS26A), rs7178572 in high mobility group 20A (HMG20A), rs2028299 in adaptor-related protein complex 3 (AP3S2), and rs4812829 in Hepatocyte Nuclear Factor 4 Alpha (HNF4A).

methodsA total of 475 subjects were genotyped for the selected SNPs in different genes using different genotyping techniques. The study subjects' age, weight, height, BMI, waist and hip circumference, serum total cholesterol, triglycerides, LDL and HDL were measured. A summation term, genetic risk score (GRS), was calculated using SPSS.

resultsThe results showed a significantly higher mean gene score in obese cases than in non-obese controls (9.1 ± 2.26 vs 8.35 ± 2.07, p = 2 × 10

conclusionIn conclusion, the use of gene score is a better way to calculate the overall genetic risk from common variants rather than individual risk variants.

Indexed as

Gene Expression RegulationGenetic Predisposition to DiseaseMultifactorial InheritancePolymorphism, Single NucleotideResearch DesignAdaptor Protein Complex 3Adaptor Proteins, Signal TransducingAdultAlpha-Ketoglutarate-Dependent Dioxygenase FTOAntigens, CDbeta-D-Galactoside alpha 2-6-SialyltransferaseBody HeightBody WeightCase-Control StudiesFatty Acid-Binding ProteinsFemaleAdaptor Protein Complex 3Adaptor Proteins, Signal TransducingAlpha-Ketoglutarate-Dependent Dioxygenase FTOAntigens, CDbeta-D-Galactoside alpha 2-6-SialyltransferaseFABP2 protein, humanFatty Acid-Binding ProteinsFTO protein, humanGRB14 protein, humanHepatocyte Nuclear Factor 4High Mobility Group ProteinsHMG20A protein, humanHNF4A protein, humanLEPR protein, humanLeptinLipoproteins, HDLLipoproteins, LDLReceptors, LeptinSialyltransferasesST6GAL1 protein, humanTriglyceridesVesicular Transport ProteinsVPS26A protein, humanGene scoreObesityPolygenicRisk variant

Identifiers

PMID30021629
PMCPMC6052513
OpenAlexW2885005825

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.