Breast cancer (BC) cells are distinguished by their capacity to reconfigure metabolism to support rapid growth and survive in hypoxic, nutrient-deficient environments. In the breast tumor microenvironment (TME), metabolic changes-including the Warburg effect, modifications in Krebs cycle intermediates, and adjusted oxidative phosphorylation-are closely associated with the dynamic signaling between tumor cells and stromal elements. Cancer-associated fibroblasts (CAFs), a diverse and adaptable group inside the stroma, significantly influence metabolic pathways, including those regulating glucose, amino acid, and lipid metabolism. Recent research underscores that the metabolic interaction between BC cells and CAFs not only promotes tumor growth and invasion but also facilitates treatment resistance. This review is aimed at consolidating the existing data on the metabolic interactions between BC cells and CAFs, highlighting molecular mechanisms and pathways that could represent potential targets for future therapies.