The sustained development of preneoplastic lesions depends on high protein intake.

The sustained development of preneoplastic lesions depends on high protein intake.
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癌前病变的持续发展依赖于高蛋白质摄入。

DOI:
10.1080/01635589209514213
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发表时间:
1992
期刊:
Nutrition and cancer
影响因子:
--
通讯作者:
Campbell,TC
Campbell,TC
中科院分区:
--
文献类型:
--
作者:
Youngman,LD;Campbell,TC

文献摘要

被引文献

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研究了连续改变两种蛋白质水平(5%和20%酪蛋白)饲料对黄曲霉毒素B1-(AFB 1)诱导的γ-谷氨酰转肽酶阳性(GGT+)癌前病灶起始后发展的影响。喂食AIN-76 A饲料(20%蛋白质)的断奶雄性Fischer 344大鼠以250 ng/kg体重(起始)的剂量胃内给予10剂AFB 1(14天给药期间每天1剂,不包括周末)。AFB 1组织清除后,大鼠被随机分配到饮食治疗组。在接下来的12周(促进),他们发展黄曲霉毒素B1诱导的GGT+癌前病变。将12周促进期细分为4个3周阶段,在此期间,大鼠在所有4个阶段(20:20:20:20)喂食含20%酪蛋白的等热量饲料,在所有4个阶段(5:5:5:5)喂食含5%酪蛋白的饲料,或连续改变酪蛋白水平(20:5:20:5和5:20:5:20)。在第3、6、9和12周处死大鼠,以检查GGT+病灶的形成对蛋白质摄入的依赖性,尽管总热量摄入更高,但饲喂5%酪蛋白饮食的动物比饲喂20%酪蛋白饮食的动物形成的GGT+病灶显著更少(p < 0.01)。同样,在干预组中,当喂食20%酪蛋白饮食时,肿瘤前发展增强,当喂食5%酪蛋白饮食时,肿瘤前发展受到抑制。这些结果表明,AFB 1诱导的癌前病变的持续发展取决于高蛋白质摄入。或者,这些结果表明,低蛋白质摄入抑制病变发展。
The effects of sequential alterations in the feeding of two levels of dietary protein (5% and 20% casein) on the postinitiation development of aflatoxin B1‐ (AFB1) induced γ‐glutamyl transpeptidase‐positive (GGT+) preneoplastic foci were examined. Weanling male Fischer 344 rats fed AIN‐76A diet (20% protein) were administered 10 intragastric doses of AFB1 (1 dose/day during the 14‐day dosing period excluding weekends) at 250 ng/kg body wt (initiation). After AFB1 tissue clearance, rats were randomly assigned to dietary treatment groups. During the next 12 weeks (promotion), they developed AFB1 induced GGT+ preneoplastic lesions. The 12‐week promotion period was subdivided into four three‐week periods, during which rats were fed isocaloric diets containing 20% casein during all four periods (20:20:20:20), 5% casein during all four periods (5:5:5:5), or sequentially altered casein levels (20:5:20:5 and 5:20:5:20). Rats were killed at 3,6,9, and 12 weeks to examine the dependence of GGT+ foci development on protein intake.Animals fed 5% casein diets developed significantly fewer (p < 0.01) GGT+ foci than animals fed 20% casein diets despite greater total caloric intake. Similarly, in the intervention groups, preneoplastic development was enhanced when the 20% casein diet was fed and inhibited when the 5% casein diet was fed. These results indicate that the sustained development of AFB1‐induced preneoplastic foci depends on a high protein intake. Alternatively, these results suggest that low protein intake inhibits lesion development.