Overview of GI Hormones - Gastrointestinal

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	↑↑ in Zollinger-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 for VIPoma and carcinoid 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