The -44 C/G (rs1800972) polymorphism of the β-defensin 1 is associated with increased risk of developing type 2 diabetes mellitus.


Journal

Molecular genetics & genomic medicine
ISSN: 2324-9269
Titre abrégé: Mol Genet Genomic Med
Pays: United States
ID NLM: 101603758

Informations de publication

Date de publication:
01 2019
Historique:
received: 03 07 2018
revised: 03 10 2018
accepted: 15 10 2018
pubmed: 15 12 2018
medline: 16 3 2019
entrez: 15 12 2018
Statut: ppublish

Résumé

The aim of this study was to establish the association of two polymorphisms of the β-defensin 1 gene (DEFB1, OMIM#602056) with the risk of developing type 2 diabetes mellitus (T2DM) in a group of Mexican patients. The 5'UTR -20 G/A, and -44 C/G polymorphisms of DEFB1 gene were genotyped by 5' exonuclease TaqMan assays in a group of 252 patients with T2DM and 522 healthy control. Under dominant and additive models adjusted for the risk factors, the C allele of the -44 C/G polymorphism was associated with increased risk of T2DM (OR = 1.63, 95% CI = 1.07-2.48, pC This study demonstrates that the C allele of -44 C/G polymorphism, as well as haplotype AC are associated with the presence of T2DM in the Mexican population. The variation in this polymorphism of the DEFB1 gene could increase the migration of the macrophages to pancreatic islets accelerate the β-cell dysfunction in T2DM.

Sections du résumé

BACKGROUND
The aim of this study was to establish the association of two polymorphisms of the β-defensin 1 gene (DEFB1, OMIM#602056) with the risk of developing type 2 diabetes mellitus (T2DM) in a group of Mexican patients.
METHODS
The 5'UTR -20 G/A, and -44 C/G polymorphisms of DEFB1 gene were genotyped by 5' exonuclease TaqMan assays in a group of 252 patients with T2DM and 522 healthy control.
RESULTS
Under dominant and additive models adjusted for the risk factors, the C allele of the -44 C/G polymorphism was associated with increased risk of T2DM (OR = 1.63, 95% CI = 1.07-2.48, pC
CONCLUSION
This study demonstrates that the C allele of -44 C/G polymorphism, as well as haplotype AC are associated with the presence of T2DM in the Mexican population. The variation in this polymorphism of the DEFB1 gene could increase the migration of the macrophages to pancreatic islets accelerate the β-cell dysfunction in T2DM.

Identifiants

pubmed: 30549243
doi: 10.1002/mgg3.509
pmc: PMC6382445
doi:

Substances chimiques

DEFB1 protein, human 0
IKZF1 protein, human 0
beta-Defensins 0
Ikaros Transcription Factor 148971-36-2

Banques de données

GENBANK
['NM_005218.3', 'NM_0055218.3', 'NC_000008.11']

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

e00509

Informations de copyright

© 2018 The Authors. Molecular Genetics & Genomic Medicine published by Wiley Periodicals, Inc.

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Auteurs

Marco Antonio Martinez-Rios (MA)

Interventional Cardiology, Instituto Nacional de Cardiología Ignacio Chávez, Mexico City, Mexico.

Gilberto Vargas-Alarcon (G)

Department of Molecular Biology, Instituto Nacional de Cardiología Ignacio Chávez, Mexico City, Mexico.

Marco Antonio Peña-Duque (MA)

Interventional Cardiology, Instituto Nacional de Cardiología Ignacio Chávez, Mexico City, Mexico.

Oscar Perez-Mendez (O)

Department of Molecular Biology, Instituto Nacional de Cardiología Ignacio Chávez, Mexico City, Mexico.

Jose Manuel Rodriguez-Perez (JM)

Department of Molecular Biology, Instituto Nacional de Cardiología Ignacio Chávez, Mexico City, Mexico.

Nonanzit Perez-Hernandez (N)

Department of Molecular Biology, Instituto Nacional de Cardiología Ignacio Chávez, Mexico City, Mexico.

Gabriel Herrera-Maya (G)

Department of Molecular Biology, Instituto Nacional de Cardiología Ignacio Chávez, Mexico City, Mexico.

Rosalinda Posadas-Sanchez (R)

Department of Endocrinology, Instituto Nacional de Cardiología Ignacio Chávez, Mexico City, Mexico.

Carlos Posadas-Romero (C)

Department of Endocrinology, Instituto Nacional de Cardiología Ignacio Chávez, Mexico City, Mexico.

Jose Manuel Fragoso (JM)

Department of Molecular Biology, Instituto Nacional de Cardiología Ignacio Chávez, Mexico City, Mexico.

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Classifications MeSH