The association of PBX1 polymorphisms with overweight/obesity and metabolic alterations in the Korean population
Nutrition Research and Practice
;
: 289-294, 2008.
Artículo
en Inglés
| WPRIM
| ID: wpr-71168
ABSTRACT
Pre-B-cell leukemia transcription factor 1 (PBX1), which is located on chromosome 1q23, was recently reported to be associated with type 2 diabetes mellitus. We examined whether single nucleotide polymorphisms (SNPs) of the PBX1 gene are associated with overweight/obesity in a Korean population. We genotyped 66 SNPs in the PBX1 gene and investigated their association with clinical phenotypes found in 214 overweight/obese subjects and 160 control subjects using the Affymetrix Targeted Genotyping chip array. Seven SNPs (g.+75186C>T, g.+78350C>A, g.+80646C>T, g.+138004C>T, g.+185219G>A, g.+191272A>C, and g.+265317T>A) were associated with the risk of obesity in three models (codominant, dominant, and recessive) (P=0.007-0.05). Haplotype 1 (CAC) and 3 (TAC) of block 3 and haplotype 2 (GGAAT) of block 10 were also strongly associated with the risk of obesity. In the control group, subjects that had homozygote for the major allele for both g.+185219G>A and g.+191272A>C showed lower high density lipoprotein-cholesterol (HDL-C) level compared to those possessing the minor allele, suggesting that the association between the homozygote for the major allele for both g.+185219G>A and g.+191272A>C and HDL-C is attributable to the increased risk of obesity. This study suggests that the PBX1 gene is a possible risk factor in overweight/obese patients.
Texto completo:
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Índice:
WPRIM (Pacífico Occidental)
Asunto principal:
Fenotipo
/
Factores de Transcripción
/
Haplotipos
/
Leucemia-Linfoma Linfoblástico de Células Precursoras B
/
Factores de Riesgo
/
Polimorfismo de Nucleótido Simple
/
Diabetes Mellitus Tipo 2
/
Alelos
/
Homocigoto
/
Obesidad
Tipo de estudio:
Estudio de etiología
/
Estudio pronóstico
/
Factores de riesgo
Límite:
Humanos
Idioma:
Inglés
Revista:
Nutrition Research and Practice
Año:
2008
Tipo del documento:
Artículo
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