Goodgame J T, Lowry S F, Reilly J J, Jones D C, Brennan M F
Am J Clin Nutr. 1979 Nov;32(11):2277-84. doi: 10.1093/ajcn/32.11.2277.
The effects of starvation on tumor and host growth were studied in growing male Fischer rats bearing methylcholanthrene-induced sarcomas. Tumor growth was evaluated by changes in weight, volume, and incorporation of tritiated methyl thymidine into tumor DNA, (dpm/microgram DNA). Host growth was followed by changes in total body weight, carcass weight, and dpm/microgram liver DNA. All periods of starvation (24 to 96 hr) caused significant decreases in host body and carcass weight and dpm/microgram liver DNA. Changes in tumor weight and tumor volume in fed and starved animals were equal. Tumor dpm/microgram DNA in starved animals increased (P less than 0.005) relative to fed controls at 48, 72, and 96 hr starvation intervals. Starvation allows continued tumor growth while host wasting occurs, and is accompanied by increased tumor dpm/microgram DNA in this system.
在生长中的雄性Fischer大鼠身上研究了饥饿对肿瘤和宿主生长的影响，这些大鼠携带着甲基胆蒽诱导的肉瘤。通过肿瘤重量、体积的变化以及氚标记甲基胸腺嘧啶掺入肿瘤DNA（每微克DNA的衰变数，dpm/μg DNA）来评估肿瘤生长。通过总体重、胴体重以及每微克肝脏DNA的衰变数来追踪宿主生长。所有饥饿期（24至96小时）均导致宿主体重、胴体重以及每微克肝脏DNA的衰变数显著下降。喂食和饥饿动物的肿瘤重量和肿瘤体积变化相同。在饥饿48、72和96小时时，饥饿动物的肿瘤每微克DNA的衰变数相对于喂食对照增加（P小于0.005）。饥饿使肿瘤持续生长而宿主消瘦，并且在该系统中伴随着肿瘤每微克DNA的衰变数增加。
