Pickens Charles A, Albuquerque Pereira Mariana de Fátima, Fenton Jenifer I
Department of Food Science and Human Nutrition, Michigan State University, East Lansing, Michigan, USA.
Eur J Cancer Prev. 2017 Nov;26(6):497-505. doi: 10.1097/CEJ.0000000000000312.
Dietary lipid intake can be associated with an increased risk for colorectal cancer depending on its composition. Carcinogenesis alters lipid metabolism to facilitate cell growth and survival. For instance, metabolites of polyunsaturated fatty acids (PUFAs) are associated with increasing colon cell proliferation. Moreover, precancerous colon lesions (i.e. adenomas) increase the risk for colorectal cancer. In this study, we investigated associations between plasma PUFAs and the number of colon polyps and polyp type (i.e. hyperplastic and adenoma). Healthy male participants (n=126) of 48-65 years of age were recruited before a routine colonoscopy screening. Plasma phospholipid (PPL) PUFAs were isolated by means of solid phase extraction and methylated. Fatty acid methyl esters were analyzed using gas chromatography. Factor analysis was used to cluster PUFAs into groups, and then generated factors and individual PUFAs were analyzed using polytomous logistic regression. In our age-adjusted and smoking-adjusted polytomous logistic regression, for each unit increase in PPL docosatetraenoic acid (DTA), individuals were 1.43 (1.00-2.06) and 1.33 (0.99-1.80) times more likely to have hyperplastic polyps and adenomas rather than no polyps, respectively. In our factor analysis, high PPL ω-6 PUFA and trans-fatty acid loading scores were associated with increased odds of adenoma presence rather than no polyps. Increases in long-chain PPL ω-6 PUFAs are associated with an increased risk for adenomas. As relative levels of DTA increase in PPLs, individuals had increased odds of having hyperplastic polyps and adenomas. Elevated conversion of ω-6 PUFAs to longer-chain ω-6s such as DTA may indicate altered PUFA metabolism at the tissue level.
饮食中的脂质摄入量可能因其成分而与结直肠癌风险增加相关。致癌作用会改变脂质代谢以促进细胞生长和存活。例如，多不饱和脂肪酸（PUFA）的代谢产物与结肠细胞增殖增加有关。此外，癌前结肠病变（即腺瘤）会增加患结直肠癌的风险。在本研究中，我们调查了血浆PUFA与结肠息肉数量及息肉类型（即增生性和腺瘤性）之间的关联。在常规结肠镜筛查前招募了年龄在48 - 65岁的健康男性参与者（n = 126）。通过固相萃取和甲基化分离血浆磷脂（PPL）中的PUFA。使用气相色谱分析脂肪酸甲酯。采用因子分析将PUFA聚类成组，然后使用多分类逻辑回归分析生成的因子和单个PUFA。在我们经年龄和吸烟调整的多分类逻辑回归中，PPL二十二碳四烯酸（DTA）每增加一个单位，个体患增生性息肉和腺瘤而非无息肉的可能性分别增加1.43（1.00 - 2.06）倍和1.33（0.99 - 1.80）倍。在我们的因子分析中，高PPL ω-6 PUFA和反式脂肪酸负荷评分与存在腺瘤而非无息肉的几率增加相关。长链PPL ω-6 PUFA的增加与腺瘤风险增加相关。随着PPL中DTA相对水平的增加，个体患增生性息肉和腺瘤的几率增加。ω-6 PUFA向更长链ω-6如DTA的转化升高可能表明组织水平上PUFA代谢发生了改变。
