Disseminated cancer cells require distinct nutrients including palmitate to effectively seed in distant organs. The major source of palmitate in the lung is surfactant, which is produced by alveolar type II (AT2) cells. However, whether overt metastases require lipids derived from AT2 cells is poorly understood. Here, we found that AT2 cells in the vicinity of metastases are reprogramed into palmitate feeder cells in mice and patients with breast cancer. Specifically, we found that the secretome of metastases alters the transcriptional landscape of AT2 cells. This includes an increase in the activity of the transcription factor sterol regulatory element-binding transcription factor 1 (SREBP-1) enhancing the expression of key de novo lipid synthesis genes including fatty acid synthase (FASN) and glycerol-3-phosphate acyltransferase 1 (GPAM). In line, we observed an increased lipid availability in the vicinity of metastases within AT2 cell-enriched tissue areas in mice and patients with breast cancer using spatial mass spectrometry imaging combined with immunohistochemistry on the same tissue section. Importantly, targeting Fasn selectively in AT2 cells and Fasn or Gpam systemically in mice was sufficient to significantly reduce metastases growth in breast cancer mouse models. In summary, we discovered that AT2 cells are recruited as lipid feeder cells to lung metastases and that targeting the lipid production of AT2 cells impairs metastases growth.