Central and peripheral glucagon-like 1 (GLP-1) systems suppress eating via independent gut-brain circuits
High fat-type microbiota is sufficient to alter appetitive feeding behavior. Bacteria to reward communication is mediated by the vagus nerve.
The vagal gut-to-brain axis is an integral component of the neuronal reward pathway
Combined activation of fat and sugar gut-brain circuits increases overeating and dopamine release
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de Lartigue Lab 