Department of Mathematics, Zhejiang University, Hangzhou, 310058, China.
Institute of Bioinformatics, Zhejiang University, Hangzhou, 310058, China.
Sci Rep. 2020 Jul 22;10(1):12136. doi: 10.1038/s41598-020-68935-x.
To reveal the impacts of smoking on genetic architecture of human body weight, we conducted a genome-wide association study on 5,336 subjects in four ethnic populations from MESA (The Multi-Ethnic Study of Atherosclerosis) data. A full genetic model was applied to association mapping for analyzing genetic effects of additive, dominance, epistasis, and their ethnicity-specific effects. Both the unconditional model (base) and conditional model including smoking as a cofactor were investigated. There were 10 SNPs involved in 96 significant genetic effects detected by the base model, which accounted for a high heritability (61.78%). Gene ontology analysis revealed that a number of genetic factors are related to the metabolic pathway of benzopyrene, a main compound in cigarettes. Smoking may play important roles in genetic effects of dominance, dominance-related epistasis, and gene-ethnicity interactions on human body weight. Gene effect prediction shows that the genetic effects of smoking cessation on body weight vary from different populations.
为了揭示吸烟对人体体重遗传结构的影响，我们对来自 MESA（动脉粥样硬化多民族研究）数据的四个种族群体的 5336 名受试者进行了全基因组关联研究。我们应用全遗传模型进行关联作图，以分析加性、显性、上位性及其种族特异性效应的遗传效应。我们同时研究了不条件模型（基础模型）和包含吸烟作为协变量的条件模型。在基础模型检测到的 10 个 SNP 涉及 96 个显著的遗传效应，占高遗传率（61.78%）。基因本体分析表明，许多遗传因素与香烟中主要化合物苯并芘的代谢途径有关。吸烟可能在人体体重的显性、显性相关上位性和基因-种族相互作用的遗传效应中发挥重要作用。基因效应预测表明，戒烟对体重的遗传效应因不同人群而异。
