Abstract: Metabolic reprogramming is a core biological hallmark of malignancies. Tumor cells reshape glucose, lipid, and amino acid metabolism to acquire adequate materials and energy for proliferation, invasion, metastasis and tumor microenvironment adaptation. Cholangiocarcinoma (CCA) exhibits distinct metabolic disorders, including Warburg effect-driven glycolytic abnormality, imbalanced fatty acid synthesis and uptake, as well as metabolic dependence on glutamine, tryptophan and other amino acids. CCA is highly malignant with obvious chemoresistance and unfavorable prognosis. Distinctive metabolic dysregulation signatures of CCA, together with their translational ramifications, have drawn wide attention. Clinically studies have progressively elucidated mechanisms underlying aberrant glycolysis, disrupted fatty acid synthesis and uptake, aminoacid metabolic addiction, and key dysregulated metabolic signaling pathways. These findings have provided new mechanistic insights into metabolism-targeted therapeutic interventions. This review systematically summarizes current advances in CCA metabolic reprogramming, expounds the regulatory roles of dysregulated glucose, lipid, and amino acid metabolism in disease progression, analyzes existing limitations and looks to the future research prospects of metabolic targeted strategies, and lays a theoretical foundation for basic research and precise clinical therapy of CCA.