Likewise, in a non-alcoholic fatty liver disease (NAFLD) model, TUDCA alleviated gut inflammatory responses via down-regulation of pro-inflammatory cytokines e.g., IL-1β, Ccl2, Ccl4, and Icam1 and improved intestinal barrier function by increasing levels of tight junction molecules and the solid chemical barrier [167]. Here, ICAM1 is linked to metabolic dysfunction-associated steatotic liver disease.