Ip C, Sinha D
Cancer Lett. 1981 Feb;11(4):277-83. doi: 10.1016/0304-3835(81)90092-6.
Female Wistar-Furth rats were fed either a high-fat (HF) or a low fat (LF) diet from weaning. The HF and LF diets contained 20% and 0.5% corn oil, respectively. Mammary gland explants from 50-day-old rats of both dietary groups were exposed to dimethylbenz[a]anthracene in organ culture before grafting to HF- or LF-hosts. A total of 4 groups were involved: LF leads to LF, HF leads to LF, LF leads to HF, and HF leads to HF, where the designations before and after the arrow describe the dietary treatment of the donor and host, respectively. Final tumor incidences were as follows: 28%, 20%, 72% and 76%, presented in the order of the above 4 groups. Tumors also appeared earlier in the HF-hosts. Results of this experiment indicate that regardless of the nutritional status of the donor, it was the fat intake of the host that governed the subsequent neoplastic growth of transformed cells, suggesting that the action of fat is primarily exerted at the promotional stage of carcinogenesis.
从断奶起,将雌性Wistar-Furth大鼠分别喂食高脂(HF)或低脂(LF)饮食。HF和LF饮食分别含有20%和0.5%的玉米油。在移植到HF或LF宿主之前,将两个饮食组50日龄大鼠的乳腺外植体在器官培养中暴露于二甲基苯并[a]蒽。总共涉及4组:LF组移植到LF宿主、HF组移植到LF宿主、LF组移植到HF宿主、HF组移植到HF宿主,其中箭头前后的名称分别描述供体和宿主的饮食处理。最终肿瘤发生率如下:上述4组依次为28%、20%、72%和76%。肿瘤在HF宿主中也出现得更早。该实验结果表明,无论供体的营养状况如何,决定转化细胞随后肿瘤生长的是宿主的脂肪摄入量,这表明脂肪的作用主要在致癌作用的促进阶段发挥。