Functional gastrointestinal disorders (FGIDs) or disorders of gut-brain interaction (DGBI) are functional gastrointestinal disorders (FGIDs), currently classified as disorders of gut-brain interaction (DGBIs), and are distinct clinical entities from gastrointestinal motility disorders (GIMDs). Nonetheless, motility abnormalities are frequently observed in FGID, often leading to diagnostic ambiguity. An important dimension in understanding these conditions is the role of gastrointestinal hormones, whose study began in the early twentieth century with the identification of secretin and gastrin. Subsequent discoveries in the 1930s included gastrone and enterogastrone, both inhibitory to gastric acid secretion and motility, and incretin, which augments insulin secretion. In the 1970s, gastric inhibitory polypeptide (GIP) was isolated, later redefined as glucose-dependent insulinotropic peptide following recognition of its incretin activity. Glucagon-like peptide-1 (GLP-1), initially considered synonymous with enterogastrone, was subsequently identified as a key regulator of gastrointestinal function. Postprandial physiology encompasses both gastrointestinal and metabolic processes. Ingestion stimulates gastrin-mediated gastric digestion, followed by the release of intestinal hormones such as secretin and cholecystokinin (CCK), which facilitate further digestion. GIP and GLP-1 enhance insulin secretion, thereby lowering postprandial glycemia and modulating gastrointestinal motility. Together with CCK, they also act centrally to suppress appetite. Dysregulation of these pathways may contribute to postprandial discomfort, dysmotility, and other negative gastrointestinal symptoms. Understanding these mechanisms offers important insights into the pathophysiology of DGBI.