Dietary (n-6) PUFA and intestinal tumorigenesis
Dietary (n-6) PUFA and intestinal tumorigenesis
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DOI：
10.1093/jn/134.12.3421s
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发表时间：
2004-12-01
影响因子：
4.2
通讯作者：
McEntee, MF
中科院分区：
文献类型：
--
作者：
Whelan, J;McEntee, MF
癌症是美国第二大死因，结直肠癌的死亡率仅次于肺癌。流行病学研究表明，饮食中的多不饱和脂肪对结直肠癌的风险有深远的影响。实验数据表明，细胞（n-6） PUFA代谢的调节可以影响疾病的进展。本文讨论了（n-6） PUFA在促进肠道肿瘤发生中的作用，以及来自不同家族的膳食PUFA如何相互作用以改变肿瘤的发生过程。饮食中减少花生四烯酸代谢的多聚脂肪酸（如（n-3）多聚脂肪酸）具有抗肿瘤特性，而那些增加花生四烯酸代谢的多聚脂肪酸，如亚油酸、γ -亚麻酸和花生四烯酸，在西方饮食中添加时，似乎不会促进肿瘤的发生，但可能会削弱其他膳食脂质的有益作用。不同膳食中多聚脂肪酸的相对贡献可能决定疾病的总体风险和进展。
Cancer is the second leading cause of death in the United States, and mortality due to colorectal cancer is only surpassed by lung cancer. Epidemiological studies demonstrate that dietary polyunsaturated fats can have a profound effect on colorectal cancer risk. Experimental data indicate that modulation of cellular (n-6) PUFA metabolism can affect the progression of the disease. This paper discusses the role (n-6) PUFA play in promoting intestinal tumorigenesis and how dietary PUFA from different families interact to modify the neoplastic process. Dietary PUFA that attenuate arachidonic acid metabolism [such as (n-3) PUFA] have antineoplastic properties, whereas those that augment arachidonic acid metabolism, such as linoleic, gamma-linolenic, and arachidonic acids do not appear to enhance tumorigenesis when added to the Western diet but may diminish the beneficial effects of other dietary lipids. It is the relative contributions of the different dietary PUFA that may determine overall risk for and progression of the disease.