Department of Nutritional Sciences, University of Toronto, Toronto, Ontario, Canada.
J Inflamm Res. 2012;5:1-6. doi: 10.2147/JIR.S27911. Epub 2012 Jan 9.
Increasing evidence suggests a role for inflammation in the development of type 2 diabetes. Elevated levels of inflammatory cytokines, including interleukin-6, have been associated with insulin resistance, and dietary lipids can increase cytokine production. The objective of this study was to determine whether a single nucleotide polymorphism near the IL6 gene (rs7801406) modifies the relationship between dietary fat and markers of insulin sensitivity.
Subjects were healthy men and women aged 20-29 years from the Toronto Nutrigenomics and Health Study. Dietary intake was estimated using a one-month semiquantitative food frequency questionnaire. Fasting blood samples were taken for genotyping and biomarker measurement.
The single nucleotide polymorphism was not associated with any of the measures of insulin sensitivity. However, it modified the relationship between total dietary fat and the homeostasis model assessment of insulin resistance (P = 0.053 for interaction). Total fat intake was positively related to HOMA-IR in individuals homozygous for the G allele (β = 0.005 ± 0.002, P = 0.03), but not among heterozygotes. There was an inverse relationship between total fat intake and HOMA-IR in individuals who were homozygous for the A allele (β = -0.012 ± 0.006, P = 0.047).
These findings suggest that dietary fat influences insulin sensitivity differently depending on genotype.
越来越多的证据表明炎症在 2 型糖尿病的发生发展中起着一定作用。包括白细胞介素-6（IL-6）在内的炎症细胞因子水平升高与胰岛素抵抗有关，膳食脂质可以增加细胞因子的产生。本研究的目的是确定 IL6 基因附近的单核苷酸多态性（rs7801406）是否改变了膳食脂肪与胰岛素敏感性标志物之间的关系。
研究对象为多伦多营养基因组学和健康研究中的 20-29 岁健康男性和女性。采用一个月的半定量食物频率问卷来估计膳食摄入量。采集空腹血样进行基因分型和生物标志物检测。
该单核苷酸多态性与任何胰岛素敏感性指标均无关。然而，它改变了总膳食脂肪与稳态模型评估的胰岛素抵抗（HOMA-IR）之间的关系（交互作用 P = 0.053）。在纯合子携带 G 等位基因的个体中，总脂肪摄入量与 HOMA-IR 呈正相关（β = 0.005 ± 0.002，P = 0.03），但在杂合子中并非如此。在纯合子携带 A 等位基因的个体中，总脂肪摄入量与 HOMA-IR 呈负相关（β = -0.012 ± 0.006，P = 0.047）。
这些发现表明，膳食脂肪对胰岛素敏感性的影响因基因型而异。
