Sylvester P W, Russell M, Ip M M, Ip C
Cancer Res. 1986 Feb;46(2):757-62.
The purpose of this investigation was to determine whether diets high in animal or vegetable fat affected mammary tumorigenesis when fed to rats only prior to and during the initiation phase of carcinogenesis. Weanling 21-day-old female Sprague-Dawley rats were divided into different dietary treatment groups and were allowed to feed and libitum on one of the following diets: 5% (normal fat) corn oil; 20% (high fat) corn oil; 20% palm oil; 20% beef tallow; or 20% lard. At 52 days of age, all rats were given p.o. 7.5 mg 7,12-dimethylbenz(a)anthracene (DMBA). One week following DMBA administration, all rats were switched to the 5% corn oil control diet and were maintained on this diet for the duration of the experiment. Rats fed a 20% lard diet during the treatment period showed a significant increase in mammary tumor incidence and number 19 weeks after DMBA administration, when compared to all other dietary treatment groups. Rats fed a 20% beef tallow diet during this same time period also demonstrated enhanced mammary tumor development, during the 10- to 19-week time period after DMBA. Mammary tumor development in rats fed 20% corn oil or palm oil diets during this treatment period was similar to that of normal fat controls. Estrogens are potent stimulators of mammary tumor growth and development in rats. Because mammary tumorigenesis was enhanced in rats fed high animal, but not vegetable fat diets, it was possible that estrogens present in animal fat might be responsible for this stimulation. Further studies demonstrated however, that increased mammary tumorigenesis in rats fed diets high in animal fat could not be explained on the basis of endocrine stimulation. Average day of vaginal opening for all groups fed 20% fat diets was similar and occurred earlier than in normal fat controls. In addition, 50- to 65-day-old rats in the different dietary treatment groups showed no differences in basal or surge levels of serum prolactin, luteinizing hormone, or estradiol. Rat diestrus uterine weight also showed no significant differences among dietary treatment groups. Thus diets containing high levels of animal fat caused little if any increased estrogenic activity in rats. In conclusion, high dietary intake of lard and beef tallow, but not vegetable fat, fed from weaning until only 1 week after DMBA administration, significantly enhances mammary tumorigenesis in rats. The mechanism(s) by which animal fat induces this stimulation is not clear, but it does not appear to result from endogenous or exogenous endocrine stimulation.
本研究的目的是确定在致癌作用起始阶段之前及期间仅喂给大鼠富含动物脂肪或植物脂肪的饮食是否会影响乳腺肿瘤的发生。将21日龄断乳的雌性斯普拉格 - 道利大鼠分成不同的饮食处理组,让它们随意进食以下饮食之一:5%(正常脂肪)玉米油;20%(高脂肪)玉米油;20%棕榈油;20%牛脂;或20%猪油。在52日龄时,给所有大鼠口服7.5毫克7,12 - 二甲基苯并(a)蒽(DMBA)。DMBA给药一周后,将所有大鼠换成5%玉米油对照饮食,并在整个实验期间维持该饮食。与所有其他饮食处理组相比,在治疗期间喂20%猪油饮食的大鼠在DMBA给药19周后乳腺肿瘤发生率和数量显著增加。在同一时期喂20%牛脂饮食的大鼠在DMBA给药后的10至19周期间也表现出乳腺肿瘤发展增强。在该治疗期间喂20%玉米油或棕榈油饮食的大鼠的乳腺肿瘤发展与正常脂肪对照组相似。雌激素是大鼠乳腺肿瘤生长和发展的有效刺激物。因为喂高动物脂肪但非植物脂肪饮食的大鼠乳腺肿瘤发生增强,所以动物脂肪中存在的雌激素可能是这种刺激的原因。然而,进一步研究表明,喂高动物脂肪饮食的大鼠乳腺肿瘤发生增加不能以内分泌刺激来解释。所有喂20%脂肪饮食组的平均阴道开口日相似,且比正常脂肪对照组更早出现。此外,不同饮食处理组中50至65日龄的大鼠在血清催乳素、促黄体生成素或雌二醇的基础水平或峰值水平上没有差异。大鼠动情期子宫重量在饮食处理组之间也没有显著差异。因此,含高水平动物脂肪的饮食在大鼠中几乎没有引起雌激素活性增加。总之,从断乳到DMBA给药后仅1周喂高猪油和牛脂但非植物脂肪的饮食,会显著增强大鼠的乳腺肿瘤发生。动物脂肪诱导这种刺激的机制尚不清楚,但似乎不是由内源性或外源性内分泌刺激引起的。