Longnecker D S, Chandar N, Sheahan D G, Janosky J E, Lombardi B
Department of Pathology, Dartmouth Medical School, Hanover, NH 03756.
Toxicol Pathol. 1991;19(1):59-65. doi: 10.1177/019262339101900107.
Groups of male Fischer 344 rats were chronically fed semipurified choline-devoid or choline-supplemented diets, high in fat (15%), and containing or not containing 0.06% phenobarbital. Atypical acinar cell nodules were observed in the pancreas of the rats, irrespective of the diet fed, with incidences varying from 38% to 100% in the various groups. No consistent differential effects of the dietary treatments on the incidence and growth of the nodules were evident, even though the diameter of the nodules tended to be greater in some of the groups fed the basal choline-devoid diet. The vast majority of the nodules were of the acidophilic type. More advanced pancreatic acinar cell lesions were observed in a few of the rats. Since the rats were not exposed to a chemical carcinogen(s), development of the nodules and of the more advanced lesions, even in rats fed the control diets, was most likely due to evolution of endogenous (spontaneous) initiated pancreatic cells, promoted primarily by the feeding of semipurified diets with a high fat content.
将雄性Fischer 344大鼠分组，长期喂食半纯化的不含胆碱或补充胆碱的高脂肪（15%）饮食，饮食中含有或不含有0.06%苯巴比妥。无论喂食何种饮食，在大鼠胰腺中均观察到非典型腺泡细胞结节，各实验组的发生率在38%至100%之间不等。尽管在喂食基础不含胆碱饮食的一些组中结节直径往往更大，但饮食处理对结节的发生率和生长没有一致的差异影响。绝大多数结节为嗜酸性类型。在少数大鼠中观察到更晚期的胰腺腺泡细胞病变。由于大鼠未接触化学致癌物，即使在喂食对照饮食的大鼠中，结节和更晚期病变的发生很可能是由于内源性（自发）启动的胰腺细胞的演变，主要是由喂食高脂肪的半纯化饮食所促进。
