Evidence map›Paper›PMID 27366637›Full record

ArticlePeerJ2016

Genetic markers of inflammation may not contribute to metabolic traits in Mexican children.

Neeti Vashi, Carolina Stryjecki, Jesus Peralta-Romero, Fernando Suarez, Jaime Gomez-Zamudio, Ana I Burguete-Garcia, Miguel Cruz, David Meyre

Open access · goldAbstract read
In one paragraph

Article in PeerJ, 2016. 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
3.3field-weighted citation impact, top 8% 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, 11 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Polymorphisms in Adipokines in Mexican Children with Obesity.International journal of endocrinology · 2019
    Article
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

8 authors at 5 institutions in 2 countries.

Neeti VashiClinical Epidemiology & Biostatistics, McMaster University , Hamilton , Canada.
Carolina StryjeckiClinical Epidemiology & Biostatistics, McMaster University , Hamilton , Canada.
Jesus Peralta-RomeroMedical Research Unit in Biochemistry, Hospital de Especialidades, Centro Médico Nacional Siglo XXI del Instituto Mexicano del Seguro Social , Mexico City , Mexico.
Fernando SuarezMedical Research Unit in Biochemistry, Hospital de Especialidades, Centro Médico Nacional Siglo XXI del Instituto Mexicano del Seguro Social , Mexico City , Mexico.
Jaime Gomez-ZamudioMedical Research Unit in Biochemistry, Hospital de Especialidades, Centro Médico Nacional Siglo XXI del Instituto Mexicano del Seguro Social , Mexico City , Mexico.
Ana I Burguete-GarciaCentro de investigación sobre enfermedades infecciosas, Instituto Nacional de Salud Pública , Cuernavaca , Mexico.
Miguel CruzMedical Research Unit in Biochemistry, Hospital de Especialidades, Centro Médico Nacional Siglo XXI del Instituto Mexicano del Seguro Social , Mexico City , Mexico.
David MeyreClinical Epidemiology & Biostatistics, McMaster University, Hamilton, Canada; Department of Pathology and Molecular Medicine, McMaster University, Hamilton, Ontario, Canada.
McMaster University · CAMexican Social Security Institute · MXCentro Medico Nacional Siglo XXI · MXHospital de Especialidades · MXInstituto Nacional de Salud Pública · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLow-grade chronic inflammation is a common feature of obesity and its cardio-metabolic complications. However, little is known about a possible causal role of inflammation in metabolic disorders. Mexico is among the countries with the highest obesity rates in the world and the admixed Mexican population is a relevant sample due to high levels of genetic diversity.

methodsHere, we studied 1,462 Mexican children recruited from Mexico City. Six genetic variants in five inflammation-related genes were genotyped: rs1137101 (leptin receptor (LEPR)), rs7305618 (hepatocyte nuclear factor 1 alpha (HNF1A)), rs1800629 (tumor necrosis factor alpha (TNFA)), rs1800896, rs1800871 (interleukin-10 (IL-10)), rs1862513 (resistin (RETN)). Ten continuous and eight binary traits were assessed. Linear and logistic regression models were used adjusting for age, sex, and recruitment centre.

resultsWe found that one SNP displayed a nominal evidence of association with a continuous trait: rs1800871 (IL-10) with LDL (beta = -0.068 ± 1.006, P = 0.01). Subsequently, we found one nominal association with a binary trait: rs7305618 (HNF1A) with family history of hypertension (odds-ratio = 1.389 [1.054-1.829], P = 0.02). However, no P-value passed the Bonferroni correction for multiple testing. DISCUSSION: Our data in a Mexican children population are consistent with previous reports in European adults in failing to demonstrate an association between inflammation-associated single nucleotide polymorphisms (SNPs) and metabolic traits.

Indexed as

Cardio-metabolic complicationsChildhoodGenetic epidemiologyInflammationMexicoObesity

Identifiers

PMID27366637
PMCPMC4924140
OpenAlexW2463219204

What OpenQuestion holds

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LicenceCC BY
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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.