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Regulation of Gastric Emptying
(Guyton and Hall Textbook of Medical Physiology, 4th South Asia Edition)
Introduction
Gastric emptying is the process by which chyme is propelled from the stomach into the duodenum through the pylorus. The rate is regulated by signals originating from both the stomach and the duodenum, with duodenal signals being far more potent. The overall purpose of this regulation is to ensure that chyme enters the small intestine no faster than it can be digested and absorbed.
1. Gastric Factors That Promote Emptying
(a) Effect of Gastric Food Volume
Increased food volume in the stomach promotes increased emptying. This is not due to a rise in intragastric pressure (because normal filling does not markedly raise pressure), but rather stretching of the stomach wall elicits local myenteric reflexes that:
- Greatly accentuate activity of the pyloric pump (peristaltic contractions of the antrum that force chyme through the pylorus), and
- Simultaneously inhibit the pyloric sphincter, allowing outflow.
(b) Role of Gastrin
Gastrin, secreted by G cells of the antrum in response to stomach distension, protein digestion products, and vagal (gastrin-releasing peptide) stimulation, has a mild stimulatory effect on gastric motility, thus modestly promoting emptying.
2. Powerful Duodenal Factors That Inhibit Gastric Emptying
These are the dominant regulatory signals, operating through two mechanisms:
(a) Enterogastric Nervous Reflexes
When chyme enters the duodenum, inhibitory reflexes are initiated from the duodenal wall and travel back to the stomach via three parallel pathways:
- Directly through the enteric nervous system in the gut wall
- Through extrinsic nerves to the prevertebral sympathetic ganglia, then via inhibitory sympathetic fibers to the stomach
- Through vagal afferents to the brainstem, which suppress excitatory vagal outflow to the stomach
Both effects of these reflexes are:
- Strong inhibition of the pyloric pump contractions
- Increased tone of the pyloric sphincter
The stimuli in the duodenum that trigger these reflexes are:
- Distension of the duodenum
- Irritation of the duodenal mucosa
- Acidity - when duodenal pH falls below ~3.5-4, emptying is reflexly blocked until acid is neutralized by pancreatic secretions
- Osmolality - both hypotonic and (especially) hypertonic fluids trigger inhibition, preventing rapid electrolyte shifts
- Breakdown products of proteins and fats in chyme
(b) Hormonal Feedback From the Duodenum
Substances in chyme entering the duodenum (especially fats and proteins) stimulate release of inhibitory hormones from the duodenal and jejunal epithelium. These hormones travel via the bloodstream to the stomach where they inhibit the pyloric pump and increase pyloric sphincter tone:
| Hormone | Source | Stimulus | Effect on Gastric Emptying |
|---|
| Cholecystokinin (CCK) | I cells, duodenum/jejunum/ileum | Fatty acids, amino acids | Strongly inhibits gastric motility - most potent inhibitory hormone |
| Secretin | S cells, duodenum | Gastric acid in duodenum | Weak delay of emptying; also inhibits gastrin release |
| Gastric Inhibitory Peptide (GIP) | K cells, duodenum/jejunum | Fat, carbohydrates | General weak inhibition of GI motility |
| GLP-1 | L cells, duodenum/ileum/colon | Carbohydrates, fats, proteins | Multiple effects that slow emptying; basis of GLP-1 agonist therapy in obesity |
3. Summary of Control
- Gastric factors (volume-induced myenteric reflexes, gastrin) provide only moderate control.
- Duodenal factors - both nervous (enterogastric reflexes) and hormonal (CCK, secretin, GIP, GLP-1) - provide the dominant, more powerful control.
- Emptying is slowed when the duodenum contains: too much chyme, excessively acid chyme, unprocessed protein or fat, hypotonic or hypertonic fluids, or irritants.
- The net result: the rate of gastric emptying is matched to the rate at which the small intestine can process chyme - ensuring adequate digestion and absorption.
Source: Guyton and Hall Textbook of Medical Physiology (ISBN 9780443111013), Chapter on Movements of the Gastrointestinal Tract, pp. 792-895.