(1) Ingestion of TRPA1 agonists. (2) On reaching small intestine, binding of TRPA1 agonists to its receptor on enterochromaffin cells (EEC) (3) present throughout the gastrointestinal tract, stimulates the secretion of serotonin or 5-HT from stored vesicles in the EEC (4). Serotonin regulates gastric motility by excitation of various intrinsic and extrinsic neurons. TRPA1 agonists when reaches duodenum, induces calcium influx inside the EEC (5), which further lead to secretion of anorectic hormone, CCK (6). In colon, L cells express TRPA1 (7), upon activation stimulates secretion of GLP-1 (8). GLP-1 maintains glucose homeostasis by different ways, one of the prominent targets of GLP-1 is pancreas. Binding of GLP-1 to its receptor on β-cells not only stimulates insulin biosynthesis (9) and secretion (12) but also enhances formation of new β-cells in pancreas. In addition to GLP-1, TRPA1 also increases insulin secretion via agonistic interactions (10). Upon activation, conformational changes in the TRPA1 structure allows calcium influx into the cell (11). Calcium ions escalate the exocytosis of insulin (12)