Table 1.
Summary of peptides and hormones involved in gastric emptying (original)
| Peptide / Hormone | Predominant Site of Synthesis/Release | Main Functions | Effects on Gastric Emptying and Other Organs in Digestive Tract |
|---|---|---|---|
| Gastrin | 17-AA peptide from gastric mucosa | - Blood-borne regulator of gastric acid secretion, interacting with somatostatin and EC cells - Regulates gastric epithelial organization, proliferation, and function |
- No direct effect on GE; increased acid secretion may be associated with modest increase in time for complete emptying |
| CCK | I cells in duodenal mucosa, particularly with fatty acids >12 carbon chain length; multiple molecular forms | - Activates vagal afferents directly and modifies the response of vagal mechanosensitive fibers to gastric and duodenal nutrients | - Relaxes the proximal stomach to increase its reservoir capacity - Inhibits GE and acid secretion - Induces gallbladder contraction and exocrine pancreatic secretion |
| Ghrelin | 28-AA peptide expressed mostly in stomach | - Growth hormone secretagogue that stimulates pituitary release of growth hormone and stimulates hypothalamic centers to increase appetite - Effects mediated through vagus nerve |
- Stimulates gastric emptying and contracts gastric fundus - Stimulates gastric acid secretion - Other actions: vasodilatation, inhibition of insulin, anti-proliferative |
| Leptin and Gastric Leptin | Leptin circulating (167 AA protein) secreted by adipose tissue, placenta, skeletal muscle; gastric leptin by fundic glands, and chief cells | - Hypothalamic regulation of feeding behavior, food intake and energy balance - Storage of fat and insulin signaling |
- Gastric leptin reduced during fasting, rapidly released after food intake by vagal cholinergic stimulation, CCK and secretin, or in response to satiety factors (e.g., CCK and insulin) |
| Amylin | Co-secreted with insulin from pancreatic β-cells | - Suppresses glucagon release in response to caloric intake - Stimulates brain satiety centers to limit caloric intake |
- Retards GE of solids |
| Glucagon | 29AA peptide secreted from pancreatic α-cells | - Maintains blood glucose by activating gluconeogenesis and glycogenolysis - Affects energy expenditure, reduces meal size |
- Retards GE of liquids - Inhibits GI motility |
| GLP-1 | Co-secreted with PYY from intestinal L cells: | - Two biologically active forms: GLP-17–37 and GLP-17–36 amide (the major circulating form) - Incretin hormone that enhances insulin secretion stimulated by oral nutrients - Control of appetite and energy intake in humans |
- Retards GE of solids and liquids and inhibits antral motility - Increases gastric reservoir capacity - Reduces postprandial glycemia - Increases satiety and fullness |
| PYY | Co-secreted with GLP-1 from ileocolonic L cells; active form PYY3–36 | - Stimulates Y2 receptors in hypothalamic ARC nucleus circuitry to regulate food intake | - Activates ileal brake and other feedback control of regional motor function, and delays GE liquids - Inhibits gastric acid, pancreatic exocrine and bile acid secretion |
| OXM | 37-AA peptide from intestinal L cells | - Acts via GLP-1 receptors to decrease food intake | - Inhibits gastric acid secretion - Modest delay in GE liquids |
AA: amino acid; ARC: arcuate nuclei of the hypothalamus; CCK: cholecystokinin; EC: enterochromaffin cells; GE: gastric emptying; GLP-1: glucagon like peptide-1; OXM: oxyntomodulin; PYY: peptide tyrosine-tyrosine