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肿瘤生长的营养调节

Nutritional modulation of tumor growth.

作者信息

Grube B J, Gamelli R L

机构信息

University of Washington, Seattle 98105.

出版信息

J Surg Res. 1988 Jul;45(1):120-7. doi: 10.1016/0022-4804(88)90030-3.

Abstract

The relationship between tumor and host tissue proliferation as a function of protein calorie deficiency followed by balanced nutritional repletion was examined in a series of C3H female mice with MA16/C tumors. Tumor and host tissue DNA synthesis was determined in animals with subcutaneously implanted tumors who were randomized to either regular diet (RD) or a totally protein-free diet (PFD) for 5 days followed by refeeding for 4, 8, 12, 24, 36, 48, or 72 hr. Animals maintained on a protein-free diet demonstrated a decrease in DNA synthetic activity in both tumor and host tissues. Following refeeding of a regular diet to animals fed the protein-free diet, resumption of DNA synthesis in tumor preceded that of liver and was greatest by four hours of refeeding. In the liver, return of DNA synthetic activity was delayed but exceeded control levels by 36 hr. Compared to our previous studies examining the effects of starvation, we found that an isocaloric protein-free diet caused a smaller decrease in tumor DNA synthetic activity and an earlier resumption in tumor proliferation with the reinstitution of a normal protein diet. These studies suggest a nutrient-specific response for tumor and host tissues with nutritional deprivation and refeeding.

摘要

在一系列患有MA16/C肿瘤的C3H雌性小鼠中,研究了蛋白质热量缺乏后再给予均衡营养补充时肿瘤与宿主组织增殖之间的关系。对皮下植入肿瘤的动物进行肿瘤和宿主组织DNA合成测定,这些动物被随机分为常规饮食(RD)组或完全无蛋白饮食(PFD)组5天,然后再喂养4、8、12、24、36、48或72小时。维持无蛋白饮食的动物在肿瘤和宿主组织中的DNA合成活性均降低。在给无蛋白饮食的动物重新喂食常规饮食后,肿瘤中DNA合成的恢复先于肝脏,并且在重新喂食4小时时最大。在肝脏中,DNA合成活性的恢复延迟,但在36小时时超过了对照水平。与我们之前研究饥饿影响的研究相比,我们发现等热量无蛋白饮食导致肿瘤DNA合成活性下降较小,并且在恢复正常蛋白质饮食后肿瘤增殖恢复较早。这些研究表明,肿瘤和宿主组织在营养剥夺和再喂养时有营养特异性反应。

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