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长期摄入咖啡对大鼠和仓鼠饮食脂肪促进的胰腺癌发生的调节作用。

Modulation of dietary fat-promoted pancreatic carcinogenesis in rats and hamsters by chronic coffee ingestion.

作者信息

Woutersen R A, van Garderen-Hoetmer A, Bax J, Scherer E

机构信息

Department of Biological Toxicology, TNO-CIVO Toxicology and Nutrition Institute, Zeist, The Netherlands.

出版信息

Carcinogenesis. 1989 Feb;10(2):311-6. doi: 10.1093/carcin/10.2.311.

Abstract

The effect of chronic coffee ingestion on dietary fat-promoted pancreatic carcinogenesis was investigated in rats and hamsters. Rats were given a single i.p. injection of 30 mg azaserine per kg body weight at 19 days of age. Hamsters were injected s.c. with 20 mg N-nitrosobis(2-oxopropyl)amine (BOP) per kg body weight at 6 and 7 weeks of age. The animals were fed a semi-purified diet high in unsaturated fat (25% corn oil) either in combination with coffee or not. Coffee was provided instead of drinking water. A separate group maintained on a diet low in unsaturated fat (5% corn oil) was included as extra controls. The rats and hamsters were given their diets and coffee after treatment with carcinogen. Terminal autopsy of rats was 15 months after azaserine treatment and of hamsters 12 months after the last injection with BOP. In rat pancreas, the numbers of adenomas and carcinomas were significantly lower in the group maintained on the combination of a high-fat diet and coffee than in the high-fat group without coffee, while in the latter group the number of adenomas and carcinomas had significantly increased as compared to the low-fat controls. In hamsters, the number of ductal/ductular adenocarcinomas had significantly increased in the high-fat group as compared to the low-fat controls. The inhibitory effect of coffee on dietary fat-promoted pancreatic carcinogenesis was also noticed in this species but was less pronounced than in rats. It was concluded that chronic coffee consumption has an inhibitory effect on dietary fat-promoted pancreatic carcinogenesis in rats and hamsters. More research is needed to elucidate the mechanism by which coffee (constituents) modulates carcinogenesis.

摘要

在大鼠和仓鼠中研究了长期摄入咖啡对膳食脂肪促进胰腺癌发生的影响。大鼠在19日龄时腹腔注射一次每千克体重30毫克的偶氮丝氨酸。仓鼠在6周龄和7周龄时皮下注射每千克体重20毫克的N-亚硝基双(2-氧代丙基)胺(BOP)。动物喂食富含不饱和脂肪(25%玉米油)的半纯化饮食,饮食中要么添加咖啡,要么不添加。用咖啡代替饮用水。另外设置一组维持在不饱和脂肪含量低(5%玉米油)的饮食作为额外对照。大鼠和仓鼠在接受致癌物处理后给予其饮食和咖啡。大鼠在偶氮丝氨酸处理后15个月进行终末尸检,仓鼠在最后一次注射BOP后12个月进行终末尸检。在大鼠胰腺中,维持高脂饮食与咖啡组合的组中腺瘤和癌的数量显著低于无咖啡的高脂组,而与低脂对照组相比,后一组中腺瘤和癌的数量显著增加。在仓鼠中,与低脂对照组相比,高脂组中导管/小导管腺癌的数量显著增加。在该物种中也观察到咖啡对膳食脂肪促进胰腺癌发生的抑制作用,但不如在大鼠中明显。得出的结论是,长期饮用咖啡对大鼠和仓鼠中膳食脂肪促进的胰腺癌发生具有抑制作用。需要更多研究来阐明咖啡(成分)调节致癌作用的机制。

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