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

doi:10.7717/peerj.2090

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

PeerJ. 2016 Jun 23:4:e2090. doi: 10.7717/peerj.2090. eCollection 2016.

Authors

Neeti Vashi¹, Carolina Stryjecki¹, Jesus Peralta-Romero², Fernando Suarez², Jaime Gomez-Zamudio², Ana I Burguete-Garcia³, Miguel Cruz², David Meyre⁴

Affiliations

¹ Clinical Epidemiology & Biostatistics, McMaster University , Hamilton , Canada.
² Medical Research Unit in Biochemistry, Hospital de Especialidades, Centro Médico Nacional Siglo XXI del Instituto Mexicano del Seguro Social , Mexico City , Mexico.
³ Centro de investigación sobre enfermedades infecciosas, Instituto Nacional de Salud Pública , Cuernavaca , Mexico.
⁴ Clinical Epidemiology & Biostatistics, McMaster University, Hamilton, Canada; Department of Pathology and Molecular Medicine, McMaster University, Hamilton, Ontario, Canada.

Abstract

Background: Low-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.

Methods: Here, 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.

Results: We 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.

Keywords: Cardio-metabolic complications; Childhood; Genetic epidemiology; Inflammation; Mexico; Obesity.

Grants and funding

David Meyre is supported by a Tier 2 Canada Research Chair in Genetics of Obesity. Miguel Cruz was supported by the Fundación IMSS A.C. and by the National Council of Science and Technology (CONACYT-México) with the grant SALUD-2013-C01-201471 (FONSEC SSA/IMSS/ISSSTE). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.