American Health Foundation, 10595, Vallalla, New York, USA,
Environ Health Prev Med. 2002 Jul;7(3):95-102. doi: 10.1265/ehpm.2002.95.
Colorectal cancer is the second most common malignancy in the Western world including the United Sates. In recent years there is a strong upward trend in colon cancer risk in Japan mainly due to Americanization of Japanese food habits. Several epidemiological studies point to a strong association between nutrient composition of the diet and cancer of the colon. The role of types of dietary fat, especially saturated fats of animal origin, n-6- and n-3-rich polyunsaturated fatty acids (PUFAs) in the etiology of colorectal cancer has become increasingly apparent. Epidemiological studies indicate a positive association between the dietary intake of saturated fat and/or animal fat and colon cancer risk and an inverse relationship between the intake of fish and fish oil rich in n-3 PUFAs and colon cancer development. Although the evidence from case-control studies and international correlational studies is not totally consistent, these inconsistencies may have arisen, at least in part, from methodological limitations. Animal, model studies have unequivocally provided evidence that the colon tumor-promoting effect of dietary fat depends on its fatty acid composition and that high dietary n-3 PUFAs lacks colon tumor-promoting effect, as compared to diets high in n-6 PUFAs or saturated fats. Diets rich in n-3 PUFAs inhibit colon carcinogenesis through the modulation of colonicras-p21, cyclooxygenase-2, and inducible nitric oxide synthase activities and apoptosis. Gene expression analysis using DNA microarrays indicates that n-3 fatty acid, docosahexaenoic acid activates cyclin-dependent kinase inhibitors such as p21, p27, p57 and p19 and inactivates antiapoptotic Bcl-2 family of genes, and prostagland in family of genes. These results suggest that decreasing the intake of n-6 PUFAs and saturated fats and increasing that of n-3 PUFAs, particularly eicosapentaenoic acid and docosahexaenoic acid has the potential to be a major component of colon cancer control.
结直肠癌是西方国家（包括美国）第二常见的恶性肿瘤。近年来，日本结肠癌的风险呈强劲上升趋势，主要归因于日本饮食习惯的美国化。几项流行病学研究表明，饮食中营养成分与结肠癌之间存在很强的关联。饮食中脂肪类型，特别是动物源性饱和脂肪、富含 n-6 和 n-3 的多不饱和脂肪酸（PUFA）在结直肠癌病因学中的作用变得越来越明显。流行病学研究表明，饮食中饱和脂肪和/或动物脂肪的摄入量与结肠癌风险呈正相关，而富含 n-3 PUFA 的鱼类和鱼油的摄入量与结肠癌的发展呈负相关。尽管来自病例对照研究和国际相关性研究的证据并不完全一致，但这些不一致可能至少部分源于方法学上的限制。动物、模型研究明确提供了证据，表明饮食脂肪的结肠肿瘤促进作用取决于其脂肪酸组成，与富含 n-6 PUFA 或饱和脂肪的饮食相比，高膳食 n-3 PUFA 缺乏结肠肿瘤促进作用。富含 n-3 PUFA 的饮食通过调节结肠ras-p21、环氧化酶-2 和诱导型一氧化氮合酶活性和细胞凋亡来抑制结肠癌的发生。使用 DNA 微阵列进行的基因表达分析表明，n-3 脂肪酸二十二碳六烯酸激活细胞周期蛋白依赖性激酶抑制剂，如 p21、p27、p57 和 p19，并使抗凋亡 Bcl-2 家族基因和前列腺素家族基因失活。这些结果表明，减少 n-6 PUFA 和饱和脂肪的摄入，增加 n-3 PUFA，特别是二十碳五烯酸和二十二碳六烯酸的摄入，有可能成为结肠癌控制的主要组成部分。
