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

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

PeerJ

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

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.

PMID: 27366637 PMCID: PMC4924140 DOI: 10.7717/peerj.2090

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

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