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The signals start with changes in gastric distention, leading to decreased acyl-ghrelin, increased deacyl-ghrelin, and increased gastric leptin.47 As food enters the duodenum, other enzymes or hormones including enterokinase, cholecystokinin (CCK), glucose-dependent insulinotropic peptide (GIP, previously called gastric inhibitory polypeptide) and glucagon are all secreted and act systemically to promote postprandial satiety (Figure 2C).48 With food entry into the small intestine, intestinal L-cells release glucagon-like peptide 1 (GLP-1), which has wide ranging systemic effects promoting satiety.49–51 Once food reaches the terminal ileum, enterocytes release peptide YY (PYY), oxyntomodulin and insulin-like peptide 5 (INSL5), which constitute the “ileal brake” and further delay gastric emptying and enteric motility.52 The cumulative effect is a central sensation of postprandial satiety, (Figure 2C)
