Evidence map›Paper›PMID 31164103›Full record

ArticleBMC medical genetics2019

Association of a genetic variant in the angiopoietin-like protein 4 gene with metabolic syndrome.

Sara Kharazmi-Khorassani, Jasmin Kharazmi-Khorassani, Azam Rastegar-Moghadam, Sara Samadi, Hamideh Ghazizadeh, Maryam Tayefi, Gordon A Ferns, Majid Ghayour-Mobarhan, Amir Avan, Habibollah Esmaily

Open access · goldAbstract read
In one paragraph

Article in BMC medical genetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.0field-weighted citation impact, top 22% 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

5 citing papers in PubMed, 8 citations in OpenAlex.

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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

10 authors at 2 institutions in 2 countries.

Sara Kharazmi-KhorassaniDepartment of Biology, Varastegar Medical University, Mashhad, Iran.
Jasmin Kharazmi-KhorassaniDepartment of Biology, Varastegar Medical University, Mashhad, Iran.
Azam Rastegar-MoghadamDepartment of Modern Sciences and Technologies, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Sara SamadiMetabolic syndrome Research center, Mashhad University of Medical Sciences, Mashhad, Iran.
Hamideh GhazizadehMetabolic syndrome Research center, Mashhad University of Medical Sciences, Mashhad, Iran.
Maryam TayefiDepartment of Modern Sciences and Technologies, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Gordon A FernsBrighton & Sussex Medical School, Division of Medical Education, Falmer, Brighton, Sussex, BN1 9PH, UK.
Majid Ghayour-MobarhanDepartment of Modern Sciences and Technologies, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Amir AvanMetabolic syndrome Research center, Mashhad University of Medical Sciences, Mashhad, Iran. avana@mums.ac.ir.
Habibollah EsmailySocial Determinants of Health Research, Center, Mashhad University of Medical Sciences, Mashhad, Iran. habib.esmaily@gmail.com.ORCID 0000-0003-4139-546X
Mashhad University of Medical Sciences · IRBrighton and Sussex Medical School · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMetabolic syndrome (MetS) is characterized by a clustering of cardiovascular risk factors that include: abdominal obesity, dyslipidemia, hypertension and glucose intolerance. Angiopoietin-like protein 4 (ANGPTL4) is a circulating peptide that is an inhibitor of lipoprotein lipase, a key enzyme in lipid metabolism. The objective of this study was to investigate the association of ANGPTL4 gene variants (E40K) with fasting serum triglyceride levels and with cardiovascular risk factors, that included the presence of MetS in 817 subjects recruited from the Mashhad stroke and heart Atherosclerosis Disorders (MASHAD) cohort Study.

methodANGPTL4 genotypes were determined using a TaqMan genotyping based real time PCR method. The association of the genetic variant with the risk of metabolic syndrome and its relationship with lipid profile were determined.

resultThe frequency of GG, GA and AA genotypes were 96.9, 2.7 and 0.4% in individuals with MetS, and 78.8, 20.8, 0.4%, in those without MetS. The GA genotype of the rs116843064 polymorphism was associated with a lower risk for MetS (e.g., OR in Codominant genetic model: 0.14, 95% CI: (0.06-0.33), p < 0.0001). Subject with an A allele had a higher risk for MetS (OR: 6.72, 95% CI: (3.05-14.82), p < 0.0001). There was a significant difference in fasted lipid profiles across the genotypes for ANGPTL4. Carriers of the AG genotype had higher levels of serum HDL-cholesterol (HDL-C) and lower TG, compared to the GG homozygotes genotype.

conclusionThe G allele at the rs116843064 polymorphic locus of the ANGPTL4 gene was associated with a lower prevalence of MetS.

Indexed as

Polymorphism, Single NucleotideAdultAllelesAngiopoietin-Like Protein 4AtherosclerosisCohort StudiesFemaleGene FrequencyGenetic Predisposition to DiseaseGenotypeHumansMaleMetabolic SyndromeMiddle AgedRisk FactorsTriglyceridesAngiopoietin-Like Protein 4ANGPTL4 protein, humanTriglyceridesANGPTL4Metabolic syndromers116843064

Identifiers

PMID31164103
PMCPMC6549319
OpenAlexW2948644801

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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.