Nat. Rev. Endocrinol. doi:10.1038/nrendo.2016.150 Figure 5 Gut bacteria-derived chemical signals that might activate intestinal satiety pathways Figure 5 | Gut bacteria-derived chemical signals that might activate intestinal satiety pathways. During their life in the gut, bacteria metabolize non-digestible fibre and digestible nutrients and produce several energy substrates such as ATP, lactate and butyrate. Upon bacterial lysis, bioactive molecules such as lipopolysaccharide (LPS) and proteins are released that continue their enzymatic activities synthesizing bioactive metabolites, such as 5-hydroxytryptamine (5HT), or acting directly as mimetics of peptide hormones, such as caseinolytic peptidase B protein homologue (ClpB). All the bacteria-derived chemical signals, along with nutrients, have direct contact with the gut epithelium that carries chemical sensors. Direct or indirect (via the enterocytes) activation of enteroendocrine cells (EECs) by bacterial signals triggers local and systemic release of peptide tyrosine tyrosine (PYY) and glucagon-like peptide 1 (GLP1), thereby transmitting satiety. Paracrine actions of bacteria-derived molecules on EEC and entrochromaffin cells, producing 5HT, might activate the enteric nervous system regulating intestinal motility and gut barrier permeability, including the access of bacterial signals to the vagal afferents. Fetissov, S. O. (2016) Role of the gut microbiota in host appetite control: bacterial growth to animal feeding behaviour Nat. Rev. Endocrinol. doi:10.1038/nrendo.2016.150