Given that CCK-induced intestinal satiety signaling was well-preserved against HF feeding in MB-treated mice of cohort 2, despite its profile of the gut microbiota, which was associated with inflammatory states, especially with Proteobacteria known to be toxic to vagal afferent neurons in vitro [41], it is more likely that the increase in butyric acid in cohort 2 was primarily derived from exogenous administration, exerting its anorexigenic action via a vagal-dependent pathway but independently of the fecal microbiota. The gene discussed is CCK; the disease is hydrops fetalis.