The intestinal phase of digestion is the third and final stage of the digestive process, occurring after the cephalic and gastric phases. It begins when chyme, a partially digested mixture of food and digestive enzymes, enters the small intestine from the stomach. This phase is crucial for nutrient absorption and involves complex hormonal and enzymatic interactions.
The arrival of the chyme in the small intestine distends the duodenum, which triggers the enterogastric reflex. This distension activates a neural response known as the enterogastric reflex which is crucial in slowing down gastric activity. This ensures that the small intestine has enough time to effectively process and absorb nutrients from the chyme.
The reflex works by inhibiting various components of the stomach's stimulatory pathways. Specifically, it reduces the activity of the submucosal and myenteric plexuses, which are neural networks that regulate gastric secretions and muscular contractions. It also diminishes parasympathetic stimulation through signals sent to the medulla, decreasing the nervous signals that promote stomach activity.
As a result of these inhibitory actions, the stomach produces less gastrin, a hormone that normally stimulates acid production and gastric motility. Gastric contractions are also reduced, meaning the mixing and emptying of stomach contents slow down. Additionally, the pyloric sphincter, the muscular valve between the stomach and small intestine, contracts to limit the further release of chyme into the small intestine. This coordinated response prevents the small intestine from becoming overwhelmed, allowing proper digestion and nutrient absorption.
Furthermore, the incoming food stimulates the enteroendocrine cells to release enterogastrones such as cholecystokinin (CCK), secretin, and gastric inhibitory peptide (GIP). CCK and GIP are activated by the lipids and carbohydrates in the food, respectively. The hormones inhibit gastric secretions and trigger the release of digestive enzymes and bile from the pancreas and gallbladder, respectively. If the food is acidic, secretin release stimulates the release of pancreatic juice to neutralize the acid and raise the pH.
After the gastric phase, the chyme from the stomach moves into the small intestine, gradually decreasing the stomach distention.
In contrast, the arrival of chyme expands the duodenal end of the small intestine, stimulating the local stretch receptors and chemoreceptors to trigger the enterogastric reflex.
This reflex inhibits stimulation of the stomach via the submucosal and myenteric plexuses, as well as parasympathetic stimulation via the medulla.
As a result, both gastrin production and gastric contractions are inhibited.
Additionally, the pyloric sphincter contracts, preventing further discharge of chyme from the stomach to the small intestine.
The incoming chyme stimulates the enteroendocrine cells scattered in the duodenal mucosa to release enterogastrone, such as cholecystokinin or CCK, secretin, and gastric inhibitory peptide or GIP.
Lipids and carbohydrates in the chyme stimulate the release of CCK and GIP. These hormones inhibit gastric secretions and trigger the pancreas to release digestive enzymes and the gallbladder to release bile.
Acidic chyme stimulates the release of secretin. This in turn, stimulates the release of pancreatic juice to increase the pH of chyme, which is favorable for digestion.
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