Emerging evidence reveals that modulation of the gut microbiota–BA axis through suppression of BSH activity, alteration of BA composition (e.g., elevated TβMCA/TUDCA), and inhibition of intestinal FXR signaling effectively enhances hepatic BA synthesis (via CYP7A1) and improves glucose/lipid homeostasis, offering novel therapeutic strategies for metabolic disorders. Here, NR1H4 is linked to metabolic disease.