A high percentage of patients with neurological diseases have significant dietary preference abnormalities (such as picky eating and texture sensitivity). Studies show Gut Microbiota (GM) mediates dietary preferences via the microbiota-gut-brain axis (MGBA), such as depression-related appetite changes linked to gut flora imbalance. GM directly or indirectly regulates dietary behavior through the vagal-mediated gut-brain signaling pathway. On the one hand, gut bacterial metabolites (such as butyrate) can directly activate vagal afferents, which project signals through the nucleus of the solitary tract (NTS) to the hypothalamic feeding center to enhance the craving for high-energy foods. The 5-hydroxytryptamine (5-HT) axis of tryptophan metabolism is also involved. On the other hand, gut microbes modulate the efficiency of tryptophan conversion to 5-HT, which in turn affects the limbic reward circuit and alters the emotion-dependent choice of specific foods, such as carbohydrate preference in depressed patients. In addition, enteroendocrine cells sense bacterial products or metabolites in the gut and regulate the activity of the vagus nerve by releasing neurotransmitters or gut hormones. These metabolites can also activate immune cells in the gut and release cytokines, which further affect the activity of the vagus nerve and indirectly regulate brain function. At the same time, change in GM will affect the integrity of the intestinal barrier, which in turn affects the function of the vagus nerve. MGBA shows promise as a target to regulate dietary preferences in neurological diseases, aiding disease management.
Hou et al. (Thu,) studied this question.