Pour P M, Groot K, Kazakoff K, Anderson K, Schally A V
Eppley Institute for Research in Cancer and Allied Diseases, University of Nebraska, Omaha 68198-6805.
Cancer Res. 1991 Sep 15;51(18):4757-61.
Controversial views exist on the link between prostatic cancer and consumption of high-fat (HF) diet. This topic was examined in experimental prostatic cancer induced in rats by N-nitrosobis(2-oxopropyl)amine (BOP). Groups of Wistar-derived MRC rats were fed a semipurified diet containing either 5% (low fat = LF) or 24.6% (HF) corn oil for life, beginning after weaning. In the short-term study, treatment with testosterone significantly increased the rate of cellular DNA synthesis (as determined by autoradiographs after tritiated thymidine injection) that was not influenced by the level of dietary fat. HF diet alone depressed the rate significantly in the dorsal lobe only. There was a significant increase in the plasma level of estradiol, a decrease in the level of luteinizing hormone, but no changes in the level of follicle-stimulating hormone (FSH) in rats treated with testosterone, with no differences between the HF and LF groups. However, HF in the absence of testosterone depressed the serum FSH level. In the carcinogenicity experiment, all rats fed HF or LF diet developed prostatic cancers (mostly adenocarcinomas). The incidence, however, was significantly higher in testosterone-treated rats. Dietary fat did not influence the incidence, histological patterns, or anatomical distribution of tumors, and there were no differences in the parameters between the HF- and LF-fed groups. Long-term administration of testosterone significantly lowered serum levels of luteinizing hormone but did not change the FSH level and affected estradiol levels to a variable extent. These values were not influenced by dietary fat. However, in the HF-BOP group, significantly higher levels of FSH were found compared with the values in the LF-BOP group. We concluded that (a) under the described experimental conditions, dietary fat, fed ad libitum, does not influence the patterns of prostatic cancer induced in rats by BOP; (b) testosterone alters the serum levels of estradiol and luteinizing hormone; and (c) both testosterone and estradiol could be involved in carcinogenesis.
关于前列腺癌与高脂（HF）饮食之间的联系存在争议性观点。本研究通过N-亚硝基双（2-氧代丙基）胺（BOP）诱导大鼠实验性前列腺癌来探讨这一话题。从断奶后开始，将Wistar品系的MRC大鼠分为两组，一组终生喂食含5%（低脂=LF）玉米油的半纯化饮食，另一组喂食含24.6%（HF）玉米油的半纯化饮食。在短期研究中，睾酮处理显著提高了细胞DNA合成速率（通过注射氚标记胸腺嘧啶后的放射自显影片测定），而这不受饮食脂肪水平的影响。单独的HF饮食仅显著降低了背叶的合成速率。在接受睾酮处理的大鼠中，雌二醇血浆水平显著升高，黄体生成素水平降低，但促卵泡激素（FSH）水平无变化，HF组和LF组之间也无差异。然而，在无睾酮的情况下，HF饮食会降低血清FSH水平。在致癌性实验中，所有喂食HF或LF饮食的大鼠都发生了前列腺癌（大多为腺癌）。然而，在接受睾酮处理的大鼠中，发病率显著更高。饮食脂肪不影响肿瘤的发病率、组织学模式或解剖分布，HF组和LF组之间的这些参数也无差异。长期给予睾酮显著降低了黄体生成素的血清水平，但未改变FSH水平，且对雌二醇水平有不同程度的影响。这些值不受饮食脂肪的影响。然而，与LF-BOP组相比，HF-BOP组的FSH水平显著更高。我们得出结论：（a）在所描述的实验条件下，随意喂食的饮食脂肪不影响BOP诱导的大鼠前列腺癌模式；（b）睾酮会改变雌二醇和黄体生成素的血清水平；（c）睾酮和雌二醇都可能参与致癌过程。
