尽管肿瘤内代谢表型与周围正常组织明显不同，但对这种异质性的重要性才刚刚被广泛认识到。结直肠癌（CRC）常被归类为华尔博格表型，即在能量产生方面，糖酵解系统优于线粒体中的氧化磷酸化（OXPHOS）。然而，这种二分法（糖酵解 vs OXPHOS）可能过于简单，不能准确代表CRC的代谢特征。因此，在这篇综述中，我们将代谢现象分解为基于源头/起源的因素，并将其重新分为两类：外在因素和内在因素。在CRC背景下，外在因素包括基于环境的因素，如缺氧、营养匮乏和肿瘤微环境，而内在因素包括基于亚群体的因素，如病理亚型和癌干细胞。这些因素在肿瘤内外形成多层次结构，以加性、占优或互斥的方式影响着它们。因此，代谢表型是一个异质且流动的现象，反映了这些因素的空间分布和时间连续性。这使得我们能够重新定义CRC中特定代谢相关因素的特征，并总结和更新我们对其异质性的积累知识。此外，我们将CRC中的肿瘤芽划分为内在因素和一种新型代谢异质性，并预测其代谢动态，提示其与循环肿瘤细胞和上皮间质转化的相似性。最后，我们讨论了使用人类肿瘤组织作为研究材料来研究和评估代谢异质性的可能性和局限性。

Although the metabolic phenotype within tumors is known to differ significantly from that of the surrounding normal tissue, the importance of this heterogeneity is just becoming widely recognized. Colorectal cancer (CRC) is often classified as the Warburg phenotype, a metabolic type in which the glycolytic system is predominant over oxidative phosphorylation (OXPHOS) in mitochondria for energy production. However, this dichotomy (glycolysis vs OXPHOS) may be too simplistic and not accurately represent the metabolic characteristics of CRC. Therefore, in this review, we decompose metabolic phenomena into factors based on their source/origin and reclassify them into two categories: extrinsic and intrinsic. In the CRC context, extrinsic factors include those based on the environment, such as hypoxia, nutrient deprivation, and the tumor microenvironment, whereas intrinsic factors include those based on subpopulations, such as pathological subtypes and cancer stem cells. These factors form multiple layers inside and outside the tumor, affecting them additively, dominantly, or mutually exclusively. Consequently, the metabolic phenotype is a heterogeneous and fluid phenomenon reflecting the spatial distribution and temporal continuity of these factors. This allowed us to redefine the characteristics of specific metabolism-related factors in CRC and summarize and update our accumulated knowledge on their heterogeneity. Furthermore, we positioned tumor budding in CRC as an intrinsic factor and a novel form of metabolic heterogeneity, and predicted its metabolic dynamics, noting its similarity to circulating tumor cells and epithelial-mesenchymal transition. Finally, the possibilities and limitations of using human tumor tissue as research material to investigate and assess metabolic heterogeneity are discussed.