Transcriptomic profiling showed upregulation of fibroblast growth factor 21, activation of the PI3K-AKT signaling pathway, and promotion of epithelial-mesenchymal transition in colorectal cancer cells, while LBPs reverse these changes.<h4>Discussion</h4>LBPs prevent CRLM associated with NAFLD by modulating the gut microbiota, enhancing butyrate production, improving hepatic metabolic homeostasis, and suppressing prometastatic signaling pathways. Here, FGF21 is linked to metabolic dysfunction-associated steatotic liver disease.