首页> 外文期刊>Nutrition and Cancer: An International Journal >Relative contribution of calories from dietary fat, carbohydrate, and fiber in the promotion of DMBA-induced mammary tumors in Sprague-Dawley rats.
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Relative contribution of calories from dietary fat, carbohydrate, and fiber in the promotion of DMBA-induced mammary tumors in Sprague-Dawley rats.

机译:饮食中的脂肪,碳水化合物和纤维中的卡路里对DMBA诱发的Sprague-Dawley大鼠乳腺肿瘤的促进作用。

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It is well known that caloric restriction inhibits, whereas excess calories promote, mammary tumorigenesis in rats. However, the relative contribution to carcinogenesis by calories derived from fat or from carbohydrate are not well established. To determine the relative effects of calories from fat or from carbohydrate, as well as any interaction of dietary fiber on the promotion of 7,12-dimethylbenz[a]anthracene-induced mammary tumors, we fed isocalorically nine diets containing different ratios of fat, carbohydrate, and fiber to female Sprague-Dawley rats treated with 7,12-dimethylbenz[a]anthracene (30/group). Under conditions of isocaloric consumption, at or near ad libitum feeding, calories from dietary fat had approximately twofold greater promoting effect on final body weight and tumor incidence than calories derived from dietary carbohydrate. Dietary fiber had an inhibitory effect on tumor development, but the effect was evident only in the high-fat groups. Logistic regression analysis of tumor incidence gave beta-coefficient estimates for the relative effects of fat, carbohydrate, and fiber of 0.866, 0.189, and -4.281, respectively. Time-to-tumor analysis by the Weibull model indicated beta-estimates of 3.016, 3.324, and 5.825 for dietary fat, carbohydrate, and fiber, respectively, indicating that fat shortens and fiber increases the length of time to tumor. The statistical model derived from these results also indicates a significant synergistic interaction of dietary fat and carbohydrate on final body weight and tumor incidence.
机译:众所周知,热量限制会抑制大鼠乳腺肿瘤的发生,而热量过多则会促进乳腺肿瘤的发生。然而,由脂肪或碳水化合物产生的卡路里对致癌作用的相对贡献尚不明确。为了确定热量来自脂肪或碳水化合物的相对影响,以及膳食纤维在促进7,12-二甲基苯并[a]蒽诱发的乳腺肿瘤中的相互作用,我们以等热量的方式喂食了九种不同脂肪比例的饮食,碳水化合物和纤维对7,12-二甲基苯并[a]蒽的雌性Sprague-Dawley大鼠(30 /组)治疗。在等热量消耗的条件下,在随意进食或接近进食的情况下,来自膳食脂肪的卡路里对最终体重和肿瘤发生率的促进作用大约是源自膳食碳水化合物的卡路里的两倍。膳食纤维对肿瘤的发展具有抑制作用,但这种作用仅在高脂人群中才明显。肿瘤发生率的逻辑回归分析得出,脂肪,碳水化合物和纤维的相对影响的β系数估计分别为0.866、0.189和-4.281。 Weibull模型进行的肿瘤时间分析表明,膳食脂肪,碳水化合物和纤维的β估计值分别为3.016、3.324和5.825,这表明脂肪缩短而纤维增加了到达肿瘤的时间。从这些结果得出的统计模型还表明,饮食脂肪和碳水化合物对最终体重和肿瘤发生率具有显着的协同作用。

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