Q. What Factors Regulate Gastric Emptying?
This post considers the factors that regulate gastric emptying.
In addition to being responsible for gastric emptying, the antral peristaltic contractions provide the driving force for gastric emptying. The amount of chyme that escapes into the duodenum with each peristaltic wave before the pyloric sphincter closes tightly depends on the strength of peristalsis.
The intensity of peristalsis can vary markedly under the influence of different signals from both the stomach and the duodenum; thus, gastric emptying is regulated by both gastric and duodenal factors.
Factors in the Stomach that Influence the Rate of Gastric Emptying
The main gastric factor that influences the strength of contraction is the amount of chyme in the stomach. Other things being equal, the stomach empties at a rate proportional to the volume of chyme in it at any given time.
Distension of the stomach triggers increased gastric motility through a direct effect of stretch on the smooth muscle as well as through involvement of the intrinsic plexuses, the vagus nerve, and the stomach hormone gastrin.
Furthermore, the degree of fluidity of the chyme in the stomach influences gastric emptying. The stomach contents must be converted into a finely divided, thick liquid form before emptying. The sooner the appropriate degree of fluidity can be achieved, the more rapidly the contents are ready to be evacuated.
Factors in the Duodenum that Influence the Rate of Gastric Emptying
Despite these gastric influences, factors in the duodenum are of primary importance in controlling the rte of gastric emptying.
The duodenum must be ready to receive the chyme and can act to delay gastric emptying by reducing peristaltic activity in the stomach until the duodenum is ready to accommodate more chyme.
Even if the stomach is distended and it content are in a liquid form it cannot empty until the duodenum is ready to deal with the chyme
The four most important factors that influence gastric emptying are:
The presence of one or more of these stimuli in the duodenum activates appropriate duodenal receptors, thereby triggering either a neural r hormonal response that puts brakes on gastric motility by reducing the excitability of the gastric smooth muscle. The subsequent reduction in antral peristaltic activity slows down the rate of gastric emptying.
- The neural response is mediated through both the intrinsic nerve plexus (short reflex) and the autonomic nerves (long reflex). Collectively, these reflexes are called the enterogastric reflex.
- The hormonal response involves the release from the duodenal mucosa of several hormones collectively known as enterogastrones. These hormones are transported b the blood to the stomach, were they inhibit antral contractions to reduce gastric emptying. The two most important enterogastrones are secretin and cholecystokinin (CCK). Secretin and CCK are major gastrointestinal hormones that perform other important functions in addition to serving as enterogastrones.
How Fat Delays Gastric Emptying
Fat is digested and absorbed more slowly than the other nutrients. Furthermore, fat digestion and absorption take place only within the lumen of the small intestine. Therefore, when fat is already present in the duodenum, further gastric emptying of more fatty stomach contents into the duodenum is prevented until the small intestine has processed the fat already there.In fact, fat is the most potent stimulus for inhibition of gastric motility. This is evident when one compares the rate of emptying of a high-fat meal (after six hours some of a bacon-and-eggs meal may still be in the stomach) with that of a protein and carbohydrate meal (a meal of lean meat and potatoes may empty in three hours).
Because the stomach secretes HCl acid, highly acidic chyme is emptied into the duodenum, where it is neutralized by sodium bicarbonate (NaHCO3) secreted into the duodenal lumen from the pancreas. Unneutralized acid irritates the duodenal mucosa and inactivates the pancreatic digestive enzymes that are secreted into the duodenal lumen. Appropriately, therefore, unneutralized acid in the duodenum inhibits further emptying of acid gastric contents until complete neutralization an be accomplished.
As molecules of protein and starch are digested in the duodenal lumen, large numbers of amino acid and glucose molecules are released. If absorption of amino acid and glucose molecules does not keep pace with the rate at which protein and carbohydrate digestion proceeds, these large numbers of molecules remain in the chyme and increase the osmolarity of the duodenal contents. Osmolarity depends o the number of molecules present, not on their size, and one protein molecule may be split into several hundred amino acid molecules, each of which has the same osmotic activity as the original protein molecule. The same holds true for large starch molecule, which yields many smaller but equally osmotically active glucose molecules. Because water is freely diffusible across the duodenal wall, it enters the duodenal lumen from the plasma as the duodenal osmolarity rises. Large volumes of water entering the intestines from the plasma lead to intestinal distension, and more importantly, circulatory disturbances ensue because of the reduction in plasma volume. To prevent these effects, gastric emptying is reflexly inhibited when the osmolarity of the duodenal contents starts to rise. Thus, the amount of food entering the duodenum for further digestion into a multitude of additional osmotically active particles is reduced until absorptive processes have had an opportunity to catch up.
Too much chyme in the duodenum inhibits the emptying of even more gastric contents, thus allowing the distended duodenum time to cope with the excess volume of chyme it already contains before it receives an additional quantity.