Kim Hyun-Jin, Min Jin-Young, Min Kyoung-Bok
Institute of Health and Environment, Seoul National University, Seoul, Korea.
Department of Preventive Medicine, Seoul National University College of Medicine, Seoul, Korea.
J Prev Med Public Health. 2016 Sep;49(5):253-259. doi: 10.3961/jpmph.16.028. Epub 2016 Jul 10.
Central obesity plays a major role in the development of many chronic diseases, including cardiovascular disease and cancer. Chronic stress may be involved in the pathophysiology of central obesity. Although several large-scale genome-wide association studies have reported susceptibility genes for central adiposity, the effects of interactions between genes and psychosocial stress on central adiposity have rarely been examined. A recent study focusing on Caucasians discovered the novel gene , which was associated with central obesity-related traits via interactions with stress levels. We aimed to evaluate gene-by-stress interaction effects on central adiposity traits, including visceral adipose tissue (VAT), in Korean adults.
A total of 1467 Korean adults were included in this study. We selected 22 single-nucleotide polymorphisms (SNPs) in the gene and analyzed their interactions with stress on central adiposity using additive, dominant, and recessive genetic modeling.
The four SNPs that had strong linkage disequilibrium relationships (rs10061900, rs10070743, rs4704967, and rs10056564) demonstrated significant interactions with the waist-hip ratio in the dominant model (<0.007). In addition, two other SNPs (rs6556377 and rs13180086) were associated with VAT by interactions with stress levels, especially in the recessive genetic model (<0.007). As stress levels increased, the mean values of central adiposity traits according to SNP genotypes exhibited gradual but significant changes (<0.05).
These results suggest that the common genetic variants for are associated with central adiposity through interactions with stress levels, emphasizing the importance of managing stress in the prevention of central obesity.
中心性肥胖在包括心血管疾病和癌症在内的多种慢性疾病的发生发展中起主要作用。慢性应激可能参与中心性肥胖的病理生理过程。尽管几项大规模全基因组关联研究报告了中心性肥胖的易感基因,但基因与心理社会应激之间的相互作用对中心性肥胖的影响很少被研究。最近一项针对高加索人的研究发现了一个新基因,该基因通过与应激水平的相互作用与中心性肥胖相关特征有关。我们旨在评估基因与应激的相互作用对韩国成年人中心性肥胖特征的影响,包括内脏脂肪组织(VAT)。
本研究共纳入1467名韩国成年人。我们在该基因中选择了22个单核苷酸多态性(SNP),并使用加性、显性和隐性遗传模型分析它们与应激对中心性肥胖的相互作用。
四个具有强连锁不平衡关系的SNP(rs10061900、rs10070743、rs4704967和rs10056564)在显性模型中与腰臀比表现出显著的相互作用(<0.007)。此外,另外两个SNP(rs6556377和rs13180086)通过与应激水平的相互作用与内脏脂肪组织相关,特别是在隐性遗传模型中(<0.007)。随着应激水平的增加,根据SNP基因型的中心性肥胖特征平均值呈现出逐渐但显著的变化(<0.05)。
这些结果表明,该基因的常见遗传变异通过与应激水平的相互作用与中心性肥胖相关,强调了在预防中心性肥胖中管理应激的重要性。