Woutersen R A, van Garderen-Hoetmer A, Longnecker D S
Carcinogenesis. 1987 Jun;8(6):833-7. doi: 10.1093/carcin/8.6.833.
The early putative pre-neoplastic lesions which arise in the Syrian golden hamster pancreas prior to the appearance of carcinomas following treatment with N-nitrosobis(2-oxopropyl)amine (BOP), have been characterized and quantitated in order to refine a protocol which permits post-initiation modulation to be evaluated within a relatively short period of time. The proposed 4-month protocol was used to investigate the modulating effects of dietary saturated fat on pancreatic carcinogenesis in hamsters. Hamsters were injected s.c. with 20 mg BOP/kg body wt at 5, 6 and 7 weeks of age. The animals were fed a low fat (LF) control diet (5% lard) or a high fat (HF) diet (20% lard) subsequent to the initiation protocol. At 4 months post-initiation, the pancreata were quantitatively examined for the number and size of putative pre-neoplastic lesions. The major attention was directed to intraductal epithelial hyperplasia of inter/intralobular or main ducts, cystic ductal complexes, tubular ductal complexes and ductal complexes that seemed to be intermediate between the latter two. The number of large ductal complexes of the intermediate and tubular category was significantly greater in hamsters fed a diet with 20% saturated fat as compared to animals maintained on 5% saturated fat. Furthermore, the number of ducts with intraductal hyperplasia was greater in the high fat group, and the proportion of such lesions judged to show atypia was also higher in this group. Dietary fat did not have a significant effect on either the cystic ductal complexes or the incidence of hyperplasia in the main pancreatic duct. These results suggest that a diet high in saturated fat enhances pancreatic carcinogenesis in the BOP-hamster model and, moreover, they suggest that a short-term (4-month) protocol may be useful for evaluation of the effects of potential modulating factors on pancreatic carcinogenesis in Syrian golden hamsters. The utility of the approach should be further evaluated and correlated with the results of long-term studies.
在用N-亚硝基双（2-氧代丙基）胺（BOP）处理后，叙利亚金仓鼠胰腺中在癌出现之前出现的早期假定的肿瘤前病变已被表征和定量，以便完善一种方案，该方案允许在相对较短的时间内评估启动后调节作用。拟议的4个月方案用于研究膳食饱和脂肪对仓鼠胰腺癌发生的调节作用。在5、6和7周龄时，给仓鼠皮下注射20mg BOP/kg体重。在启动方案之后，给动物喂食低脂（LF）对照饮食（5%猪油）或高脂（HF）饮食（20%猪油）。在启动后4个月，对胰腺中假定的肿瘤前病变的数量和大小进行定量检查。主要关注的是小叶间/小叶内或主胰管、囊性导管复合体、管状导管复合体以及似乎介于后两者之间的导管复合体的导管内上皮增生。与维持在5%饱和脂肪饮食的动物相比，喂食20%饱和脂肪饮食的仓鼠中，中等和管状类别的大导管复合体数量明显更多。此外，高脂组中导管内增生的导管数量更多，并且该组中被判定为显示异型性的此类病变的比例也更高。膳食脂肪对囊性导管复合体或主胰管增生的发生率均无显著影响。这些结果表明，高饱和脂肪饮食会增强BOP-仓鼠模型中的胰腺癌发生，此外，它们还表明短期（4个月）方案可能有助于评估潜在调节因子对叙利亚金仓鼠胰腺癌发生的影响。该方法的实用性应进一步评估，并与长期研究结果相关联。
