| Hormone | Source | Action | Regulation | Notes |
| Gastrin | G cells (stomach-antrum) | ↑ gastric H+ secretion↑ growth of gastric mucosa ↑ gastric motility | ↑ by stomach distension↑ by amino acids, small peptides↑ by vagal stimulation (GRP)↓ by stomach pH < 1.5↓ by somatostatin | ↑↑ in Zollinger-Ellison syndromePhenylalanine and tryptophan are potent stimulators |
| Cholecystokinin (CCK) | I cells (duodenum, jejunum) | ↑ pancreatic secretion↑ gallbladder contraction and relaxation of sphincter of Oddi↓ gastric emptying | ↑ by amino acids, small peptides↑ by fatty acids | A patient with cholelithiasis (gallstones) experiences worsened pain after fatty food ingestion due to ↑ release of CCK |
| Secretin | S cells (duodenum) | ↑ pancreatic HCO3– secretion↑ biliary HCO3– secretion↓ gastric H+ secretion | ↑ by H+ in duodenum↑ by fatty acids in duodenum | ↑ HCO3– neutralizes gastric H+ in duodenum, essential for fat digestion (pancreatic lipases have pH optimums between 6 and 8) |
| Somatostatin | D cells ( GI mucosa)delta cells (endocrine pancreas) | ↓ gastric H+ and pepsinogen secretion↓ pancreatic and small intestine fluid secretion↓ gallbladder contraction↓ insulin and glucagon release | ↑ by H+↓ by vagal stimulation | Inhibitory hormoneAntigrowth hormone effects (digestion and absorption of substances needed for growth)Somatostatin is treatment for VIPoma and carcinoid tumors |
| Glucose-dependent insulinotropic peptide (GIP) | K cells (duodenum, jejunum) | exocrine: ↓ gastric H+ secretionendocrine: ↑ insulin secretion by pancreatic beta cells | ↑ by fatty acids↑ by amino acids↑ by oral glucose | An oral glucose load is utilized by cells more rapidly than an equivalent IV glucose load |
| Vasoactive intestinal polypeptide (VIP) | parasympathetic ganglia in sphincters, gallbladder, and small intestine | ↑ intestinal water and electrolyte secretion↑ relaxation of intestinal smooth muscle and sphincters | ↑ by distention and vagal stimulation↓ by adrenergic input | VIPoma is a non-α, non-β islet cell pancreatic tumor that secretes VIP and causes copious diarrhea |
| Nitric oxide (NO) | – | ↑ smooth muscle relaxation ( lower esophageal sphincter) | – | Loss of NO secretion is implicated in ↑ lower esophageal tone of achalasia |
| Motilin | small intestine (upper duodenum) | increases GI motilityproduces migrating motor complexes (MMCs) | ↑ in fasting state | – |
| Ghrelin | P/D1 cells (stomach) | ↑ growth hormone, ACTH, cortisol, and prolactin secretion | ↑ before meals↓ after meals | Regulates hunger, meal initiationLost following gastric bypass surgeryAssociated with hyperphagia in Prader-Willi |
| Neuropeptide-Y | neurons of sympathetic nervous system | ↑ appetite, ↓ energy expenditure | Ghrelin ↑ releaseLeptin ↓ release | – |
| Glucagon-like peptide 1 (GLP-1) | L cells (endocrine cells of the intestinal epithelium) | ↑ glucose-induced insulin secretion from pancreatic β-cells↓ glucagon secretion↓ GI motility and secretionsPromotes satiety | Secreted in response to meal intakeDegraded by dipeptidyl peptidase IV | – |
| Leptin | Adipocytes in adipose tissue | ↓ appetite | proportional to total body fat mass | deficiency results in hyperphagia |
