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Genetic markers of inflammation may not contribute to metabolic traits in Mexican children
Author(s) -
Neeti Vashi,
Carolina Stryjecki,
Jesús PeraltaRomero,
Fernando SuárezObando,
Jaime Gómez-Zamudio,
Ana I. Burguete-García,
Miguel Cruz,
David Meyre
Publication year - 2016
Publication title -
peerj
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.927
H-Index - 70
ISSN - 2167-8359
DOI - 10.7717/peerj.2090
Subject(s) - biology , inflammation , genetics , genetic marker , evolutionary biology , computational biology , gene , immunology
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.

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