Meguid M M, Muscaritoli M, Beverly J L, Yang Z J, Cangiano C, Rossi-Fanelli F
Department of Surgery, University Hospital, State University of New York Health Science Center, Syracuse 13210.
JPEN J Parenter Enteral Nutr. 1992 Nov-Dec;16(6 Suppl):56S-59S. doi: 10.1177/014860719201600604.
Tumor growth is accompanied by an anorexia mediated by humoral factors that appear to influence appetitive mechanisms in the brain. Because tumor resection is followed by resumption of normal food intake, the circulating anorexigenic substance(s) are produced either by the neoplastic tissue or by the host in response to the tumor. Increased levels of plasma free tryptophan and plasma ammonia have been proposed to mediate cancer anorexia. With animal models, it is often difficult to ascertain whether changes in food intake depend upon metabolic changes or the progressively increasing tumor mass per se. The feeding patterns and biochemical changes that occur during tumor growth were evaluated in 96 male Fischer rats that were inoculated with 10(6) methylcholanthrene sarcoma cells or saline (controls). Rats were placed into metabolic cages equipped with an Automated Computerized Rat Eater Meter to continuously determine meal size and meal number. Plasma free tryptophan and ammonia were evaluated 6, 10, 16, 18, 22, and 26 days after tumor inoculation. Anorexia developed by day 17-18, when food intake started to decrease via a decrease in meal size but not meal number and reached 60% of control by day 26. However, long before anorexia developed, free tryptophan was significantly higher 6 days after tumor inoculation, and the greatest increase occurred after 18 days. Ammonia did not differ from control at any time. Data confirm tumor-associated increases in plasma free tryptophan that occurred before the manifestation of anorexia and support a possible role of brain serotonin in cancer anorexia.
肿瘤生长伴随着由体液因子介导的厌食症，这些体液因子似乎会影响大脑中的食欲机制。由于肿瘤切除后食物摄入量恢复正常，循环中的厌食物质是由肿瘤组织产生的，或者是宿主对肿瘤的反应产生的。血浆游离色氨酸和血浆氨水平升高被认为是介导癌症厌食症的原因。在动物模型中，通常很难确定食物摄入量的变化是取决于代谢变化还是肿瘤本身的逐渐增大。在96只接种了10(6)甲基胆蒽肉瘤细胞或生理盐水（对照组）的雄性Fischer大鼠中，评估了肿瘤生长过程中出现的进食模式和生化变化。将大鼠放入配备自动计算机化大鼠进食量计的代谢笼中，以连续测定每餐食量和餐数。在接种肿瘤后的第6、10、16、18、22和26天评估血浆游离色氨酸和氨。厌食症在第17 - 18天出现，此时食物摄入量开始通过每餐食量的减少而下降，但餐数不变，到第26天时降至对照组的60%。然而，在厌食症出现之前很久，接种肿瘤后6天血浆游离色氨酸就显著升高，最大增幅出现在18天后。氨在任何时候都与对照组没有差异。数据证实了在厌食症出现之前血浆游离色氨酸与肿瘤相关的增加，并支持大脑血清素在癌症厌食症中可能发挥的作用。
