Kuno Toshiya, Hirose Yoshinobu, Yamada Yasuhiro, Yoshida Koujirou, Qiao Zheng, Katayama Masaki, Sakata Keiko, Hara Akira, Sugie Shigeyuki, Mori Hideki
Department of Pathology, Gifu University School of Medicine, 40 Tsukasa-Machi, Gifu 500-8705, Japan.
Oncol Rep. 2003 May-Jun;10(3):699-703.
Epidemiological studies and laboratory animal model assays suggest that a high intake of dietary fat promotes mammary carcinogenesis as well as colon tumorigenesis. Fat intake in the United States traditionally includes high amounts (30% of total caloric intake) of saturated fatty acids (SFAs) compared to polyunsaturated fatty acids (PUFAs). A recent study suggested that a high-fat mixed-lipid diet (HFML), which simulates the mixed-lipid and high SFAs composition of the average American diet, strongly promotes rat colon carcinogenesis, even when compared to another high-fat diet containing PUFA-rich corn oil. On the other hand, some reports suggest that a high-fat diet rich in n-6 PUFAs promotes mammary carcinogenesis more strongly than a high-fat diet rich in SFAs. Therefore, the present study was designed to compare the effects of HFML, high-fat corn oil diet (HFCO) that is rich in n-6 PUFAs, and a low-fat corn oil diet (LFCO) on 7,12-dimethylbenz[a]anthracene (DMBA)-induced mammary carcinogenesis in female F344 rats. At 7 weeks of age, female F344 rats intended for carcinogen treatment received a gavage of DMBA at a dose level of 65 mg/kg of body weight. Beginning 1 week after carcinogen treatment, groups of rats were then maintained on experimental diets containing LFCO, HFCO or HFML. All rats were evaluated weekly by palpation of mammary tumors and sacrificed 20 weeks after the DMBA treatment. Palpable tumors of mammary glands were detected at the 8, 11, and 19 weeks in the HFCO, HFML and LFCO groups, respectively. Histopathological observation revealed that the incidence and number of mammary tumors in the HFCO group were significantly higher than in the LFCO group. Rats on the HFML diet tended towards a higher incidence and number of mammary tumors compared with the LFCO group, although the correlation was not statistically significant. These results suggest that, for this animal model, both the HFCO and HFML diets promote DMBA-induced mammary carcinogenesis when compared to the LFCO diet, and that the HFCO diet is more tumor-promotional than the HFML diet.
流行病学研究和实验动物模型试验表明，高膳食脂肪摄入会促进乳腺癌变以及结肠癌发生。与多不饱和脂肪酸（PUFAs）相比，美国传统的脂肪摄入量中饱和脂肪酸（SFAs）含量较高（占总热量摄入的30%）。最近一项研究表明，高脂肪混合脂质饮食（HFML）模拟了美国普通饮食的混合脂质和高SFAs组成，即使与另一种富含PUFA的玉米油的高脂肪饮食相比，也能强烈促进大鼠结肠癌发生。另一方面，一些报告表明，富含n-6 PUFAs的高脂肪饮食比富含SFAs的高脂肪饮食更能强烈促进乳腺癌变。因此，本研究旨在比较HFML、富含n-6 PUFAs的高脂肪玉米油饮食（HFCO）和低脂肪玉米油饮食（LFCO）对7,12-二甲基苯并[a]蒽（DMBA）诱导的雌性F344大鼠乳腺癌变的影响。7周龄时，准备接受致癌物处理的雌性F344大鼠以65 mg/kg体重的剂量经口灌胃DMBA。在致癌物处理1周后，将大鼠分组并维持在含有LFCO、HFCO或HFML的实验饮食中。每周通过触诊乳腺肿瘤对所有大鼠进行评估，并在DMBA处理20周后处死。在HFCO、HFML和LFCO组中，分别在第8、11和19周检测到可触及的乳腺肿瘤。组织病理学观察显示，HFCO组乳腺肿瘤的发生率和数量显著高于LFCO组。与LFCO组相比，HFML饮食的大鼠乳腺肿瘤的发生率和数量有升高趋势，尽管相关性无统计学意义。这些结果表明，对于该动物模型，与LFCO饮食相比，HFCO和HFML饮食均促进DMBA诱导的乳腺癌变，且HFCO饮食比HFML饮食更具肿瘤促进作用。
