Garcia-Garcia Maritza Roxana, Morales-Lanuza María Antonieta, Campos-Perez Wendy Yareny, Ruiz-Madrigal Bertha, Maldonado-Gonzalez Monserrat, Vizmanos Barbara, Hernandez-Cañaveral Ivan, Yañez-Sanchez Irinea, Roman Sonia, Panduro Arturo, Martinez-Lopez Erika
Deparment of Molecular Biology in Medicine, Civil Hospital of Guadalajara 'Fray Antonio Alcalde', Guadalajara, Jalisco, Mexico.
J Nutrigenet Nutrigenomics. 2014;7(4-6):212-24. doi: 10.1159/000371801. Epub 2015 Mar 12.
BACKGROUND/AIMS: Single nucleotide polymorphisms (SNPs) in the ADIPOQ gene could explain the adiponectin level. However, the knowledge about the influence of genetic and lifestyle factors is not sufficient. The aim was to analyze whether the effect of the -11391G/A SNP in the ADIPOQ gene is modulated by lifestyle factors in Mexican subjects.
A cross-sectional study was performed in which 394 participants were analyzed. Genetic, anthropometric, biochemical, dietary, clinical and physical activity parameters were measured. Statistical analysis was performed with SPSSv19 software.
The distribution of the -11391G/A SNP genotypes was 55.6 and 44.4% for GG and AG, respectively. The adiponectin level was modulated by the -11391G/A SNP in response to the body mass index (BMI); A allele carriers showed a higher adiponectin level compared to G homozygous carriers but only in the minor BMI tertile group (p=0.032). Adiponectin level variability was explained by gender [(r)=1.5, 95% CI 1.1-1.9, p=0.000], insulin resistance [(r)=-1.2, 95% CI -0.8 to -1.6, p=0.000], physical activity [(r)=0.6, 95% CI 0.2-0.9, p=0.002] and monounsaturated fat intake [(r)=0.5, 95% CI 0.38-1.0, p=0.047].
The adiponectin level was modulated by the interaction between BMI and -11391G/A SNP; this suggests that the lifestyle rather than genetic factors modulates serum adiponectin.
背景/目的:脂联素基因中的单核苷酸多态性(SNP)可解释脂联素水平。然而,关于遗传和生活方式因素影响的了解尚不充分。本研究旨在分析墨西哥人群中脂联素基因-11391G/A SNP的效应是否受生活方式因素的调节。
进行了一项横断面研究,分析了394名参与者。测量了遗传、人体测量、生化、饮食、临床和身体活动参数。使用SPSSv19软件进行统计分析。
-11391G/A SNP基因型的分布中,GG型和AG型分别为55.6%和44.4%。脂联素水平受-11391G/A SNP与体重指数(BMI)相互作用的调节;与G纯合子携带者相比,A等位基因携带者的脂联素水平更高,但仅在BMI较低三分位数组中如此(p = 0.032)。脂联素水平的变异性可由性别[(r)= 1.5,95%可信区间1.1 - 1.9,p = 0.000]、胰岛素抵抗[(r)= -1.2,95%可信区间 -0.8至 -1.6,p = 0.000]、身体活动[(r)= 0.6,95%可信区间0.2 - 0.9,p = 0.002]和单不饱和脂肪摄入量[(r)= 0.5,95%可信区间0.38 - 1.0,p = 0.047]来解释。
脂联素水平受BMI与-11391G/A SNP之间相互作用的调节;这表明生活方式而非遗传因素调节血清脂联素。