INSERM UMR 866, Center Lipids, Nutrition, Cancer, LabEx LipSTIC, ANR-11-LABX-0021, Dijon, France.
Cancer Epidemiol Biomarkers Prev. 2013 Aug;22(8):1417-27. doi: 10.1158/1055-9965.EPI-13-0168. Epub 2013 May 23.
Although dietary fatty acids may influence colorectal carcinogenesis, few studies have examined the association with adenoma risk. We assessed the association between biomarkers of dietary fatty acids or metabolism of fatty acids and the risk of colorectal adenomas in a nested case-control study from the French E3N-EPIC cohort.
Among 13,106 women without prevalent cancer who completed the diet history questionnaire and who provided blood samples, 328 cases of adenomatous polyp were identified during an average of 6.6-year follow-up and randomly matched to 619 polyp-free colonoscopy controls. Erythrocyte membrane phospholipid fatty acid concentrations were determined by gas chromatography. Adjusted ORs for risk of colorectal adenomas with increasing concentrations of fatty acids were calculated using conditional logistic regression, separately for advanced and nonadvanced adenomas.
Associations were stronger with advanced than nonadvanced adenomas. High concentration of pentadecanoate plus heptadecanoate acids were inversely associated with the risk of advanced adenomas [highest vs. lowest tertile: OR(T3vsT1) = 0.40 (95% confidence interval (CI) 0.20-0.79); P(trend) = 0.009]. Oleic acid was associated with an increased risk of advanced adenomas [OR(T3vsT1) = 2.32 (1.16-4.64); P(trend) = 0.018]. Some polyunsaturated fatty acids were associated with the risk of advanced adenomas, either positively for di-homo-γ-linolenate [OR(T3vsT1) = 2.07 (1.15-3.72); P(trend) = 0.013], or negatively for eicosapentaenoic and docosahexaenoic acids [OR(T3vsT1) = 0.50 (0.27-0.93); P(trend) = 0.044 and OR(T3vsT1) = 0.50 (0.26-0.96); P(trend) = 0.028, respectively].
A specific erythrocyte membrane phospholipid fatty acid profile, presumably reflecting both a complex dietary pattern and altered fatty acid metabolism, is associated with advanced colorectal adenoma risk.
Adenomas could be a target for primary prevention of colorectal cancer, using interventional strategy based on lipidomic profile of patients.
尽管膳食脂肪酸可能会影响结直肠癌的发生，但很少有研究探讨其与腺瘤风险的关系。我们评估了法国 E3N-EPIC 队列中的嵌套病例对照研究中膳食脂肪酸生物标志物或脂肪酸代谢与结直肠腺瘤风险之间的关联。
在完成饮食史问卷且提供血液样本的 13106 名无前期癌症的女性中，在平均 6.6 年的随访期间发现 328 例腺瘤性息肉病例，并随机匹配 619 例无息肉结肠镜对照。通过气相色谱法测定红细胞膜磷脂脂肪酸浓度。使用条件逻辑回归，分别针对进展期和非进展期腺瘤，计算随着脂肪酸浓度增加，结直肠腺瘤风险的调整比值比（OR）。
与非进展期腺瘤相比，与进展期腺瘤的相关性更强。高浓度的十五烷酸和十七烷酸与进展期腺瘤的风险呈负相关[最高三分位数与最低三分位数（T3vsT1）：OR（T3vsT1）=0.40（95%置信区间（CI）0.20-0.79）；P（趋势）=0.009]。油酸与进展期腺瘤的风险增加相关[OR（T3vsT1）=2.32（1.16-4.64）；P（趋势）=0.018]。一些多不饱和脂肪酸与进展期腺瘤的风险相关，对于二高-γ-亚麻酸呈正相关[OR（T3vsT1）=2.07（1.15-3.72）；P（趋势）=0.013]，而对于二十碳五烯酸和二十二碳六烯酸呈负相关[OR（T3vsT1）=0.50（0.27-0.93）；P（趋势）=0.044 和 OR（T3vsT1）=0.50（0.26-0.96）；P（趋势）=0.028]。
特定的红细胞膜磷脂脂肪酸谱，可能反映了复杂的饮食模式和脂肪酸代谢的改变，与结直肠腺瘤进展的风险相关。
腺瘤可能是结直肠癌一级预防的靶点，可以基于患者的脂质组学特征采用干预策略。
