Eating disorders could be treated by modulating gut microbiota Brain Food Reward GutBrainAxis Obesity gastrointestinal UCLouvain_be frontiersin
By Nidhi Saha, BDSAug 17 2022Reviewed by Benedette Cuffari, M.Sc. In a recent Frontiers in Neuroscience journal study, researchers describe how the gut-brain axis facilitates communication between the gastrointestinal tract and brain to regulate food consumption behaviors. Some of the key mediators involved in this process include gastrointestinal hormones, bioactive lipids, neurotransmitters, bacterial metabolites, and compounds.
Therapeutic approaches aimed toward optimizing the gut microbiota could alter food reward perceptions and, as a result, modify food intake behaviors. These newer approaches for tackling obesity are likely to provide better success rates. The homeostatic control of food intake upon peripheric signals. Orexigenic hormones or neurotransmitters are in green; anorexigenic hormones or neurotransmitters are in red.
The reward system controlling non-homeostatic food intake. Nac, nucleus accumbens; GABA, γ-aminobutyric acid; VTA, ventral tegmental area. Created with BioRender.com. Importantly, other organs contribute to the homeostatic control of food intake. For example, adipose tissue and the pancreas secrete adiponectin and amylin, respectively, both of which assist in controlling blood glucose levels.
Several genes are involved in the homeostatic control of food, which is often altered in morbidly obese individuals. For example, some genes appear to cause the overexpression of leptin within adipose tissues in obese individuals, which can subsequently cause leptin resistance to arise.
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