Overview 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 ↑↑ inZollinger-Ellison syndrome Phenylalanine 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 hormone Antigrowth hormone effects (digestion and absorption of substances needed for growth) Somatostatin is treatment forVIPoma andcarcinoid tumors Glucose-dependent insulinotropic peptide (GIP) K cells (duodenum, jejunum) exocrine: ↓ gastric H+ secretion endocrine: ↑ 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 motility produces 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 initiation Lost following gastric bypass surgery Associated with hyperphagia in Prader-Willi Neuropeptide-Y neurons of sympathetic nervous system ↑ appetite, ↓ energy expenditure Ghrelin ↑ release Leptin ↓ 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 secretions Promotes satiety Secreted in response to meal intake Degraded by dipeptidyl peptidase IV - Leptin Adipocytes in adipose tissue ↓ appetite proportional to total body fat mass deficiency results in hyperphagia