Bipolar disorder (BD) is a chronic mood disorder characterized by recurrent episodes of depression and (hypo-) mania. The gut microbiome is a potential avenue through which metabolic signaling, inflammatory pathways and environmental factors influence mood disorders via the gut-brain axis. Fecal microbiota transplantation (FMT) is a translational tool for investigating the connections between the gut microbiome and the brain, and there is evidence that FMT from humans to mice can induce changes in affective behavior. In this study, we compared the behavior, gut-brain metabolomic profiles, and inflammatory marker expression in two groups of female C57BL/6J mice, one receiving FMT from a human donor with BD in a mixed episode (HAM-D = 20, YMRS = 14) and another receiving FMT from a mentally healthy control donor without BD (HAM-D and YMRS = 0). We demonstrate that mice receiving FMT from individuals with BD had an increased abundance of Bacteroidota and decreased abundances of Parabacteroides merdae and Akkermansia muciniphila associated with altered levels of fecal metabolites, short-chain fatty acids, and related gut hormone expression relative to mice receiving control donor FMT. BD mice also exhibited differential regulation of several metabolites and inflammatory markers in the amygdala, with glycine being the most prominently affected. Furthermore, BD mice displayed increased anxiety-like behavior and decreased sociability, indicating that aspects of the behavioral phenotype of BD are transferable from humans to mice via FMT. Taken together, these findings implicate gut-brain signaling in the physiological and behavioral changes observed in our BD-FMT mouse model.