Bartolí R, Fernández-Bañares F, Navarro E, Castellà E, Mañé J, Alvarez M, Pastor C, Cabré E, Gassull M A
Department of Gastroenterology, Hospital Universitari Germans Trias i Pujol, Carretera del Canyet s/n, 08916 Badalona, Spain.
Gut. 2000 Feb;46(2):191-9. doi: 10.1136/gut.46.2.191.
Animal model studies have shown that the colon tumour promoting effect of dietary fat depends not only on the amount but on its fatty acid composition. With respect to this, the effect of n9 fatty acids, present in olive oil, on colon carcinogenesis has been scarcely investigated.
To assess the effect of an n9 fat diet on precancer events, carcinoma development, and changes in mucosal fatty acid composition and prostaglandin (PG)E(2) formation in male Sprague-Dawley rats with azoxymethane induced colon cancer.
Rats were divided into three groups to receive isocaloric diets (5% of the energy as fat) rich in n9, n3, or n6 fat, and were administered azoxymethane subcutaneously once a week for 11 weeks at a dose rate of 7.4 mg/kg body weight. Vehicle treated groups received an equal volume of normal saline. Groups of animals were colectomised at weeks 12 and 19 after the first dose of azoxymethane or saline. Mucosal fatty acids were assessed at 12 and 19 weeks. Aberrant crypt foci and the in vivo intracolonic release of PGE(2) were assessed at week 12, and tumour formation at week 19.
Rats on the n6 diet were found to have colonic aberrant crypt foci and adenocarcinomas more often than those consuming either the n9 or n3 diet. There were no differences between the rats on the n9 and n3 diets. On the other hand, administration of both n9 and n3 diets was associated with a decrease in mucosal arachidonate concentrations as compared with the n6 diet. Carcinogen treatment induced an appreciable increase in PGE(2) formation in rats fed the n6 diet, but not in those fed the n3 and n9 diets.
Dietary olive oil prevented the development of aberrant crypt foci and colon carcinomas in rats, suggesting that olive oil may have chemopreventive activity against colon carcinogenesis. These effects may be partly due to modulation of arachidonic acid metabolism and local PGE(2) synthesis.
动物模型研究表明,膳食脂肪对结肠肿瘤的促进作用不仅取决于其含量,还取决于其脂肪酸组成。关于这一点,橄榄油中所含的n9脂肪酸对结肠癌发生的影响鲜有研究。
评估n9脂肪饮食对用氧化偶氮甲烷诱导结肠癌的雄性斯普拉格-道利大鼠癌前事件、癌发展以及黏膜脂肪酸组成和前列腺素(PG)E2形成变化的影响。
将大鼠分为三组,分别给予富含n9、n3或n6脂肪的等热量饮食(脂肪提供5%的能量),并以7.4毫克/千克体重的剂量率每周皮下注射一次氧化偶氮甲烷,共11周。溶剂处理组注射等量生理盐水。在首次注射氧化偶氮甲烷或生理盐水后的第12周和第19周,将动物分组进行结肠切除术。在第12周和第19周评估黏膜脂肪酸。在第12周评估异常隐窝病灶和体内结肠内PGE2的释放,在第19周评估肿瘤形成。
发现食用n6饮食的大鼠比食用n9或n3饮食的大鼠更常出现结肠异常隐窝病灶和腺癌。食用n9和n3饮食的大鼠之间没有差异。另一方面,与n6饮食相比,n9和n3饮食的摄入均与黏膜花生四烯酸浓度降低有关。致癌物处理使食用n6饮食的大鼠的PGE2形成明显增加,但食用n3和n9饮食的大鼠没有增加。
膳食橄榄油可预防大鼠异常隐窝病灶和结肠癌的发生,表明橄榄油可能对结肠癌发生具有化学预防活性。这些作用可能部分归因于对花生四烯酸代谢和局部PGE2合成的调节。