本文报道在不同营养状态下胰岛素样生长因子－１（ＩＧＦ－Ⅰ）对肿瘤及宿主蛋白质代谢的影响。Ｓｐｒａｇｕｅ－Ｄａｗｌｅｙ大鼠皮下接种Ｗａｌｋｅｒ２５６癌肉瘤细胞后分组予以禁食或静脉高营养（ｔｏｔａｌｐａｒｅｎｔｅｒａｌｎｕｔｒｉｔｉｏｎ，ＴＰＮ），分别观察外源性ＩＧＦ－Ⅰ短期应用对肿瘤及宿主蛋白质代谢的改变。结果表明，在禁食状态下，小剂量的外源性ＩＧＦ－Ⅰ对荷瘤宿主蛋白质代谢无明显影响，而肿瘤蛋白质合成增加，提示对肿瘤的生长具有促进作用。单纯ＴＰＮ显著改变肿瘤及宿主的蛋白质代谢，整体蛋白质的氧化和合成增加、分解减少，肝脏蛋白质合成和分解均减少，肌肉蛋白合成增加，机体能量消耗也增加。同时，肿瘤蛋白质合成增加，分解代谢则无影响，提示肿瘤的生长加速。然而在ＴＰＮ支持下应用小剂量ＩＧＦ－Ⅰ，肿瘤蛋白质的合成和荷瘤宿主的静息能量消耗并不增加，宿主肌肉蛋白质分解则明显减少，反映了有利于宿主营养代谢的改善而又不促进肿瘤的生长 This article reports the effect of insulin-like growth factor-1 (IGF-I) on tumor and host protein metabolism in different nutritional states. Sprague-Dawley rats were subcutaneously inoculated with Walker256 carcinosarcoma cells and fasted either by fasting or total parenteral nutrition (TPN). The changes of tumor and host protein metabolism after short-term application of exogenous IGF-I were observed. The results showed that in the fasted state, the low-dose exogenous IGF-I had no significant effect on the metabolism of tumor-bearing host proteins, while the increase in tumor protein synthesis suggested a role in the promotion of tumor growth. TPN alone significantly alters protein metabolism in the tumor and host, increases overall protein oxidation and synthesis, reduces breakdown, reduces synthesis and breakdown of liver protein, increases muscle protein synthesis, and increases body energy expenditure. At the same time, tumor protein synthesis increased and catabolism had no effect, suggesting that tumor growth accelerated. However, with the use of low-dose IGF-I under the support of TPN, the synthesis of tumor proteins and the resting energy expenditure of the tumor-bearing host do not increase, and the protein degradation of the host muscle is significantly reduced, reflecting the improvement of the nutrition metabolism of the host without promoting Tumor growth