肿瘤发生、发展过程中，其代谢表型通常会发生改变。除了传统营养物质（葡萄糖、脂质、谷氨酰胺）来源的代谢重 编程外，乳酸、乙酸、酮体、外源蛋白质等也能被肿瘤细胞重新摄取利用。健康的肠道菌群维持着体内稳态和肠道正常功能，在 调控宿主能量代谢、促进食物消化以及调节免疫等方面有着重要的生理意义。然而肠道菌群的代谢产物能够重塑肿瘤营养微 环境，迫使肿瘤细胞通过改变代谢方式支持自身增殖和转移。本文将从肿瘤代谢重编程的营养物质来源以及肠道菌群参与的 代谢重编程调控两个方面进行系统阐述：一方面，肿瘤代谢发生重新编程，肿瘤细胞不断摄取周围环境的各种营养物质，为自 身的生长增殖提供能量；另一方面，肠道菌群经其代谢产物调控肿瘤代谢重编程进程，同时，肿瘤代谢产物又可以反馈于肠道 菌群，影响肠道生态平衡。了解肿瘤代谢重编程的发生机制，揭示肠道菌群与肿瘤代谢之间的相互作用显得尤为重要，这将为 未来寻找有效的代谢靶向的肿瘤预防和治疗方案以及潜在药物奠定良好的理论基础。

Metabolic phenotypes are often altered during the process of tumor onset and development. This metabolic reprogramming mode not only comprises traditional nutrient sources (glucose, lipids, glutamine), but also lactate, acetate, ketone bodies and exogenous proteins can also be re⁃ingested and utilized by cancer cells. A healthy gut microbiota maintains homeostasis and normal intestinal function, and has important physiological significance in regulating host energy metabolism, promoting food digestion, and modulating immunity. However, the metabolites of the gut microbiota are capable of reshaping the nutritional microenvironment of tumors, forcing cancer cells to support their own proliferation and metastasis by changing their metabolic manners. In this paper, we systematically reviewed the nutrient sources involved in tumor metabolic reprogramming and its regulation by gut microbiota. On the one hand, tumor metabolism is reprogrammed, and tumor cells continuously absorb various nutrients from the surrounding environment to provide energy for their own growth and proliferation. On the other hand, the gut microbiota modulates the process of tumor metabolic reprogramming through its metabolites. At the same time, tumor metabolites possess a feed⁃back effect on the gut microbiota and then the intestinal ecological balance. It is particularly crucial to understand the mechanism of tumor metabolic reprogramming and reveal the interaction between the gut microbiota and tumor metabolism. This will provide a good theoretical basis for the exploration of effective metabolic targeted prevention and treatment strategy and potential drugs for cancer in the future.