Department of Nutrition, School of Public Health, University of Sao Paulo, Dr. Arnaldo Avenue 715, São Paulo 01246-904, Brazil.
Department of Nutrition, School of Public Health, University of Sao Paulo, Dr. Arnaldo Avenue 715, São Paulo 01246-904, Brazil.
Clin Nutr. 2018 Apr;37(2):659-666. doi: 10.1016/j.clnu.2017.02.009. Epub 2017 Feb 17.
BACKGROUND & AIMS: Metabolic syndrome (MetS) is a cluster of interrelated risk factors for type 2 diabetes mellitus, and cardiovascular disease, with underlying inflammatory pathophysiology. Genetic variations and diet are well-known risk factor for MetS, but the interaction between these two factors is less explored. The aim of the study was to evaluate the influence of interaction between SNP of inflammatory genes (encoding interleukin (IL)-6, IL-1β and IL-10) and plasma fatty acids on the odds of MetS, in a population-based cross-sectional study.
Among participants of the Health Survey - São Paulo, 301 adults (19-59 y) from whom a blood sample was collected were included. Individuals with and without MetS were compared according to their plasma inflammatory biomarkers, fatty acid profile, and genotype frequency of the IL1B (rs16944, rs1143623, rs1143627, rs1143634 and rs1143643), IL6 (rs1800795, rs1800796 and rs1800797) and IL10 (rs1554286, rs1800871, rs1800872, rs1800890 and rs3024490) genes SNP. The influence of gene-fatty acids interaction on MetS risk was investigated.
IL6 gene SNP rs1800795 G allele was associated with higher odds for MetS (OR = 1.88; p = 0.017). Gene-fatty acid interaction was found between the IL1B gene SNP rs116944 and stearic acid (p inter = 0.043), and between rs1143634 and EPA (p inter = 0.017). For the IL10 gene SNP rs1800896, an interaction was found for arachidonic acid (p inter = 0.007) and estimated D5D activity (p inter = 0.019).
The IL6 gene SNP rs1800795 G allele is associated with increased odds for MetS. Plasma fatty acid profile interacts with the IL1B and IL10 gene variants to modulate the odds for MetS. This and other interactions of risk factors can account for the unexplained heritability of MetS, and their elucidation can lead to new strategies for genome-customized prevention of MetS.
代谢综合征（MetS）是 2 型糖尿病和心血管疾病的一组相互关联的危险因素，其潜在的病理生理学基础为炎症。遗传变异和饮食是 MetS 的已知危险因素，但这两个因素之间的相互作用研究较少。本研究旨在评估炎症基因（编码白细胞介素（IL）-6、IL-1β 和 IL-10）的 SNP 与血浆脂肪酸之间的相互作用对代谢综合征发生几率的影响，这是一项基于人群的横断面研究。
在圣保罗健康调查的参与者中，纳入了 301 名成年人（19-59 岁），他们的血液样本被采集。根据他们的血浆炎症生物标志物、脂肪酸谱和 IL1B（rs16944、rs1143623、rs1143627、rs1143634 和 rs1143643）、IL6（rs1800795、rs1800796 和 rs1800797）和 IL10（rs1554286、rs1800871、rs1800872、rs1800890 和 rs3024490）基因 SNP 的基因型频率，比较有和无 MetS 的个体。研究了基因-脂肪酸相互作用对 MetS 风险的影响。
白细胞介素 6 基因 SNP rs1800795 的 G 等位基因与 MetS 的发生几率增加相关（OR=1.88；p=0.017）。发现白细胞介素 1B 基因 SNP rs116944 与硬脂酸之间存在基因-脂肪酸相互作用（p inter=0.043），rs1143634 与 EPA 之间存在基因-脂肪酸相互作用（p inter=0.017）。对于白细胞介素 10 基因 SNP rs1800896，发现花生四烯酸（p inter=0.007）和估计的 D5D 活性（p inter=0.019）与基因存在交互作用。
白细胞介素 6 基因 SNP rs1800795 的 G 等位基因与 MetS 的发生几率增加相关。血浆脂肪酸谱与 IL1B 和 IL10 基因变异相互作用，调节 MetS 的发生几率。这种以及其他危险因素的相互作用可以解释 MetS 未被解释的遗传性，其阐明可以为 MetS 的基于基因组的预防提供新策略。
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