What controls gut motility?

What controls gut motility?

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I have two different papers. One claims that gut motility is reduced by stimulation of the Opioid κ and δ receptors. The receptors are activated by Morphine and certain derivatives, specifically Codeine, Fentanyl, Hydromophone, Methadone, and Oxycodone.

The second paper claims that gut motility is reduced by blocking the 5-HTb3 receptors. Antagonists or competitors to the 5-HTb3 receptors being Morphine and certain derivatives.

Are these two different theories, two different action mechanisms, or am I missing something?

They are two different mechanisms.

Opium is arguably one of the oldest herbal medicines, being used as analgesic, sedative and antidiarrheal drug for thousands of years. These effects mirror the actions of the endogenous opioid system and are mediated by the principal μ-, κ- and δ-opioid receptors. In the gut, met-enkephalin, leu-enkephalin, β-endorphin and dynorphin occur in both neurons and endocrine cells. When released, opioid peptides activate opioid receptors on the enteric circuitry controlling motility and secretion. As a result, inhibition of gastric emptying, increase in sphincter tone, induction of stationary motor patterns and blockade of peristalsis ensue. Opioid receptors in the gastrointestinal tract

Roles of 5-HT in health include control of normal gut motor activity, secretion, and sensation, and regulation of food intake and cell growth. Abnormalities of serotonergic function contribute to symptom genesis in functional bowel disorders, inflammatory and infectious diseases of the gut, emetic responses to varied stimuli, obesity, and dysregulation of cell growth. Therapies acting as agonists or antagonists of 5-HT receptors or that modulate 5-HT reuptake play prominent roles in managing these conditions… Serotonin and the GI tract.

When discussing the control of gut motility there is more to mention than the use of serotonergics and opioids - a number of peptide and nonpeptide neurotransmitters are important. Somatostatin and nitric oxide are two examples which each happen be inhibitory of intestinal motor function, but by two completely different mechanisms. A bit of understanding in cell biology, specifically cell signalling would be helpful to fully grasp this, but the former acts by inhibiting the release of Acetylcholine and Substance P while the latter increases levels of cAMP/cGMP. And don't forget about the basics when it comes to motor control - the cholinergics and adrenergics (including dopamine) are logical opposites.


Leung, P.S. 2014, The Gastrointestinal System: Gastrointestinal, Nutritional and Hepatobiliary Physiology, Springer, 19/03/2018,

Causes and Risk Factors of Gastric Motility Disorders

Priyanka Chugh, MD, is a board-certified gastroenterologist in practice with Trinity Health of New England in Waterbury, Connecticut.

In normal digestion, food is moved through the digestive tract by rhythmic contractions called peristalsis. This movement is called "gastric motility." When someone suffers from a digestive motility disorder, these contractions don't work the way they should, potentially leading to a variety of problems.

Intestinal walls consist of layers of muscles. In normal conditions, these muscles contract and relax in a coordinated, rhythmic fashion that propels food from the esophagus to the stomach, and through the intestine to the anus.

But, in the presence of a motility disorder, these contractions don't occur in a coordinated fashion. This results in food not passing through the intestine properly.

What Causes Stomach Motility Issues?

In order to fix a problem, you typically need to understand the cause of that problem.

There are probably a hundred different causes for stomach motility issues. The culprit could be found at almost any point within the digestive system.

But many times, the cause is associated with a condition. So if you’ve been diagnosed with any of the below, oftentimes you’ll be able to identify the cause.

Here are 15 associated stomach motility conditions.

Bacteria in the gut have a direct line to the brain

Three-dimensional view of mouse intestine shows sensory neurons in areas exposed to high-levels of microbial compounds.

With its 100 million neurons, the gut has earned a reputation as the body’s “second brain”—corresponding with the real brain to manage things like intestinal muscle activity and enzyme secretions. A growing community of scientists are now seeking to understand how gut neurons interact with their brain counterparts, and how failures in this process may lead to disease.

Now, new research shows that gut bacteria play a direct role in these neuronal communications, determining the pace of intestinal motility. The research, conducted in mice and published in Nature, suggests a remarkable degree of communication between our nervous system and the microbiota. It may also have implications for treating gastrointestinal conditions.

“We describe how microbes can regulate a neuronal circuit that starts in the gut, goes to the brain, and comes back to the gut,” says Rockefeller’s Daniel Mucida, associate professor and head of the Laboratory of Mucosal Immunology. “Some of the neurons within this circuit are associated with irritable bowel syndrome, so it is possible that dysregulation of this circuit predisposes to IBS.”

The work was led by Paul A. Muller, a former graduate student in the Mucida lab.

How microbes control motility

To understand how the central nervous system senses microbes within the intestines, Mucida and his colleagues analyzed gut-connected neurons in mice that lacked microbes entirely, so-called germ-free mice that are raised from birth in an isolated environment, and given only food and water that has been thoroughly sterilized. They found that some gut-connected neurons are more active in the germ-free mice than in controls and express high levels of a gene called cFos, which is a marker for neuronal activity.

This increase in neuronal activity, in turn, causes food to move more slowly than usual through the digestive tract of the mice. When the researchers treated the germ-free mice with a drug that silences these gut neurons, they saw intestinal motility speed up.

It’s unclear how the neurons sense the presence of gut microbes, but Mucida and his colleagues found hints that the key may be a set of compounds known as short-chain fatty acids, which are made by gut bacteria. They found that lower levels of these fatty acids within the guts of mice were associated with greater activity of the gut-connected neurons. And when they boosted the animal’s gut levels of these compounds, the activity of their gut neurons decreased. Other microbial compounds and gut hormones that change with the microbiota were also found to regulate neuronal activity, suggesting additional players in this circuit.

Neurons in control

Further experiments revealed a conundrum, however. The scientists saw that the particular type of gut-connected neurons activated by the absence of microbes did not extend to the exposed surface of the intestines, suggesting that they cannot sense the fatty acid levels directly.

So Mucida and his colleagues decided to trace the circuit backwards and found a set of brainstem neurons that show increased activity in the germ-free mice. When the researchers manipulated control mice to specifically activate these same neurons, they saw an increase in the activity of the gut neurons and a decrease in intestinal motility.

The researchers continued to work backwards, next focusing their attention on the sensory neurons that send signals from the intestines to the brainstem. Their experiments revealed these sensory neurons extended to the interface of areas of the intestine that are exposed to high-levels of microbial compounds, including fatty acids. They turned off these neurons, to mimic what happens in germ-free mice that lack the fatty acids, or associated gut signals, and observed activated neurons in the brainstem, as well as activation of the gut neurons that control intestinal motility.

“We traced the whole loop and saw that neurons outside the intestines can be controlled by what happens inside the intestines,” Mucida says. “It is plausible that the circuit identified here could be involved in additional gut-brain bidirectional interactions, which could influence several intestinal as well as neurological diseases, including IBS and even behavioral abnormalities.”

Gut bacteria could be responsible for side effect of Parkinson's drug

IMAGE: Levodopa (top right) is converted by gut bacteria to DHPPA (middle right), which has an inhibitory effect on the acetylcholine-induced gut motility (depicted on the bottom right). These findings are. view more

Credit: University of Groningen

Bacteria in the small intestine can deaminate levodopa, the main drug that is used to treat Parkinson's disease. Bacterial processing of the unabsorbed fractions of the drug results in a metabolite that reduces gut motility. These findings were described in the journal BMC Biology on 20 October by scientists from the University of Groningen. Since the disease is already associated with constipation, processing of the drug by gut bacteria may worsen gastrointestinal complications.

Patients with Parkinson's disease are treated with levodopa, which is converted into the neurotransmitter dopamine in the brain. Levodopa is absorbed in the small intestine, although not all of it. Eight to ten per cent travels further to a more distal part of the gut and this percentage increases with age and administered drug dosage. In this distal part of the gut, it may encounter bacterial species such as Clostridium sporogenes, which can deaminate (remove an -NH2 group from) aromatic amino acids.

Intestinal motility

'Last year, other scientists demonstrated this bacterium's deamination activity on aromatic amino acids,' says Sahar El Aidy, assistant professor of Microbiology at the University of Groningen. El Aidy knew that the chemical structure of levodopa is similar to that of the aromatic amino acid tyrosine. 'This suggested that the bacterium could metabolize levodopa, which may affect the intestinal motility of individuals with Parkinson's disease.'

Studies by El Aidy and her research team revealed that the bacterium C. sporogenes does indeed break down levodopa into 3-(3,4-dihydroxy phenyl)propionic acid (DHPPA). 'This process involves four steps, three of which were already known. However, we uncovered the initial step, which is mediated by a transaminase enzyme.'

Next, the team investigated whether DHPPA has an effect on motility of the distal small bowel, using an ex vivo model system for gut motility. Gut motility was induced by adding acetylcholine, after which DHPPA was added. 'Within five minutes, this decreased the motility by 69 percent, rising to 73 percent after ten to fifteen minutes.' This clearly showed that the levodopa metabolite can reduce gut contractions, which could lead to constipation.

To test whether these findings are relevant to Parkinson's disease patients, Sebastiaan van Kessel, a PhD student in El Aidy's research team, tested patients' stool samples for the presence of DHPPA. 'Because it is also produced as a breakdown product of coffee and fruits, we compared samples from patients with those from healthy controls with a comparable diet,' explains El Aidy. The result showed significantly higher DHPPA levels in stool samples of Parkinson's disease patients who were treated with levodopa. To confirm that this metabolite resulted from the presence and activity of the gut bacterium C. sporogenes, or other gut bacteria capable of anaerobic deamination, bacteria from stool samples were cultured and fed with the precursor of DHPPA. This experiment showed that the bacteria can indeed metabolize levodopa to produce DHPPA.

All of these results suggest that a residue of the drug levodopa, which is not absorbed early on in the gut, can be metabolized by gut bacteria into DHPPA, which then reduces the motility of the distal gut. As constipation is already one of the symptoms of Parkinson's disease, it is unfortunate that the drug to treat the symptoms can itself further reduce gut motility due to gut bacterial metabolization. 'However, now that we know this, it is possible to look for inhibitors of the enzymes in the deamination pathway identified in our study.'

Simple Science Summary

Individuals with Parkinson's disease are treated with the drug levodopa, which is absorbed in the gut. Microbiologist Sahar El Aidy and her research team from the University of Groningen discovered that some of the levodopa is broken down by bacteria in the gut into a substance (DHPPA) that reduces gut motility. Therefore, the drug that is used to treat Parkinson's disease can cause constipation, which is unfortunate because constipation is already a symptom of the disease. However, the results of this study could inspire the discovery of inhibitors that stop the breakdown of levodopa into DHPPA.

Reference: Sebastiaan P. van Kessel, Hiltje R. de Jong, Simon L. Winkel, Sander S. van Leeuwen, Sieger A. Nelemans, Hjalmar Permentier, Ali Keshavarzian and Sahar El Aidy: Gut bacterial deamination of residual levodopa medication for Parkinson's disease BMC Biology, 20 October 2020

Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.

Differences Between the Myenteric and Submucosal Plexuses

The myenteric plexus consists mostly of a linear chain of many interconnecting neurons that extends the entire length of the gastrointestinal tract. A section of this chain is shown in Figure 62–4.

Because the myenteric plexus extends all the way along the intestinal wall and because it lies between the longitudinal and circular layers of intestinal smooth muscle, it is concerned mainly with controlling muscle activity along the length of the gut. When this plexus is stimulated, its principal effects are (1) increased tonic contraction, or “tone,” of the gut wall, increased intensity of the rhythmical contractions, slightly increased rate of the rhythm of contraction, and (4) increased velocity of conduction of excitatory waves along the gut wall, causing more rapid move-ment of the gut peristaltic waves.

The myenteric plexus should not be considered entirely excitatory because some of its neurons are inhibitory their fiber endings secrete an inhibitorytransmitter, possibly vasoactive intestinal polypeptide or some other inhibitory peptide. The resulting inhibitory signals are especially useful for inhibiting some of the intestinal sphincter muscles that impede movement of food along successive segments of the gastrointestinal tract, such as the pyloric sphincter, which controls emptying of the stomach into the duo-denum, and the sphincter of the ileocecal valve, which controls emptying from the small intestine into the cecum.

The submucosal plexus, in contrast to the myenteric plexus, is mainly concerned with controlling function within the inner wall of each minute segment of the intestine. For instance, many sensory signals originate from the gastrointestinal epithelium and are then integrated in the submucosal plexus to help control local intestinal secretion, local absorption, and local contraction of the submucosal muscle that causesvarious degrees of infolding of the gastrointestinal mucosa.

So, how exactly do gut bacteria control our mind?

Neuroscientist John Cryan points to research which shows that the bacteria themselves are able to send signals through the vagus nerve. Remember that the vagus nerve is what connects the Enteric Nervous System (the gut’s brain) and the Central Nervous System. Additionally, gut bacteria may release metabolites which get into the bloodstream and then into the Central Nervous System, thus affecting our actions, mood, and function. (Source)

This isn’t just theory. Research has shown how bacterial changes in the gut can produce anxiety-like symptoms, and how people with certain changes to their gut flora crave certain foods. Even the introduction of a signal strain of bacteria into mice has shown drastic changes in their anxiety levels. (Source)


L'objet de ce travail est de préciser le rôle des hormones gastro-intestinales dans le contrôle de la motilité digestive. Au niveau de l'estomac proximal, la cholécystokinine (CCK), la gastrine et la sécrétine inhibent les contractions. Elles diminuent la pression intragastrique et ralentissent l'évacuation gastrique des liquides. Le polypeptide inhibiteur gastrique (GIP), le glucagon et le polypeptide intestinal vasoactif (VIP) ralentissent peutêtre aussi la vidange gastrique, car ils inhibent également les contractions gastriques proximales mais cet effet sur la vidange n'a pas été étudié. A l'opposé, la motiline augmente les contractions de l'estomac proximal et accélère l'évacuation gastrique de liquides. Les contractions de l'estomac distal sont stimulées par la gastrine, la CCK et la motiline elles sont inhibées par la sécrétine, le GIP et le VIP. Il est possible que la modulation des contractions gastriques par ces hormones influence le brassage intragastrique des aliments et l'évacuation des solides mais ceci n'a pas été étudié. Les contractions du pylore sont accrues par la CCK et la sécrétine, et cet effet stimulant est bloqué par la gastrine. Cette stimulation devrait, en principe, réduire le reflux duodéno-gastrique mais ceci n'a pas non plus été démontré. Au niveau de l'intestin grêle, la CCK, la gastrine, la motiline, le VIP et le glucagon stimulent les contractions, qui sont inhibées par la sécrétine. La CCK et la motiline accélèrent le transit intestinal le VIP et le glucagon le ralentissent. Les bouffées cycliques de contractions gastroduodénales qui surviennent dans l'état de jeûne sont associées a une élévation des concentrations plasmatiques de motiline les contractions caractéristiques de l'état postprandial sont reproduites par l'administration de gastrine et de CCK. A ce jour, la participation de ces effets hormonaux dans les mécanismes physiologiques n'a été démontrée que pour la CCK sur l'estomac proximal et pour la gastrine sur l'estomac distal.

Intestinal Motility

The ability of the walls of the small and large intestines to contract and relax allows for the movement of intestinal contents from one site to another. Specific motility patterns subserve the functions of each intestinal segment. In addition, specialized muscle regions, or sphincters, retard the passage of intestinal contents in a controlled fashion at specific sites.

Role and Significance in the Small Intestine

As we have learned from previous chapters, the primary role of the small intestine is to digest the various components of the meal and to absorb the resulting nutrients into the bloodstream or lymphatic system. The motility patterns observed in the small intestine are profoundly altered by eating. The duration of such changes depends on the caloric load and the type of nutrients ingested, with lipids having the most durable effect. During the fed state, many of the motility patterns in the small intestine are designed not to propel the intestinal contents aborally, but rather to mix the contents with the various digestive secretions and prolong their exposure to the absorptive epithelium. The muscle layers of the small intestine interact to provide for “two steps forward and one step back,” retaining the intestinal contents long enough to provide for efficient extraction of most or all useful substances. In general, therefore, the motility functions of the small intestine control the rate of nutrient absorption. The speed with which the contents are propelled also varies along the length of the small intestine. Movement is fastest in the duodenum and jejunum, providing for rapid mixing and propulsion of the contents both orally and aborally. Motility then slows in the ileum, providing additional time for the absorption of slowly permeable nutrients, and particularly, lipids. Then, once the meal is digested and absorbed, the small intestine converts to the migrating motor complex (MMC) we also discussed for the stomach, a pattern of relative quiescence punctuated by propulsive motility patterns that expel undigested residues through the small intestine and into the colon.

Role and Significance in the Colon

The functions of the colon are quite distinct from those of the small intestine. Thus, while the colon does engage in some limited digestion and salvage of nutrients from undigested residues, with the cooperation of its endogenous flora, the primary functions of the colon are to extract and reclaim water from the intestinal contents, and to process the feces for elimination. As a result, even in the fasted state, the motility functions of particularly the ascending and transverse colon are considerably more biased toward mixing the contents and retaining them for prolonged periods, and the colon does not participate in the MMC. On the other hand, periodically, large propulsive contractions sweep through the colon, transferring its contents to the rectum and ultimately promoting the urge to defecate.

Functional Anatomy

Muscle Layers

The small intestine, a hollow tube approximately 600 cm in length in a normal adult, is surrounded by two overlapping muscle layers that together make up the muscularis externa. A layer of circular muscle is found closest to the mucosa, overlaid by a longitudinal muscle layer. Taken together, these muscle layers can produce most, if not all, of the stereotypical motility patterns of the small intestine. There is also a thin layer of muscle sandwiched between the mucosa and submucosa, the muscularis mucosa, but the contribution of this muscle layer to the bulk motility properties of the small intestine is unclear. Instead, it may confer specific motility functions on mucosal structures, such as the villi.

The functions of the circular and longitudinal muscle layers are closely integrated. In part, this derives from the fact that they engage in a high level of electrical coupling. Structures known as gap junctions, which permit small second messengers and electrical signals to be communicated between adjacent cells, mean that stimulation of one smooth muscle cell can rapidly be transmitted to its neighbors, without the need for additional neural input. The function of the two muscle layers is also coordinated by the activity of interstitial cells of Cajal. These cells undergo rhythmic cycles of depolarization, related to oscillations in intracellular calcium concentration. As in the stomach, these cells provide the pacemaker function that dictates the basal electrical rhythm, or slow waves, that ultimately control the rate and locations of phasic contractions of the smooth muscle. In the duodenum, the basal electric rhythm occurs at a rate of 12 cycles per minute (cpm), although this slows as one moves distally to 7–8 cpm in the distal ileum. Interstitial cells of Cajal are essential for the peristaltic reflex in the small intestine (and to a lesser extent in the colon) and their numbers may be reduced under conditions associated with slowed transit, such as constipation.

The large intestine also contains both circular and longitudinal muscle layers that regulate its motility, but the anatomic arrangement of these differs somewhat from that seen in the small intestine. In the ascending, transverse, and descending colon, the circular muscle layer is overlaid by three long nonoverlapping bands of longitudinal muscle oriented at 120° to each other, known as the taeniae coli . Electrical coupling between the circular muscle and taeniae coli is less effective than seen in between the corresponding muscle layers in the small intestine, which likely contributes to less effective propulsive motility. The circular muscle layer is also contracted intermittently to divide the colon into functional segments known as haustra . The speed of impulse propagation is faster in the circular muscle of the colon than in the longitudinal layers, allowing for these segmenting ring contractions. Note that the haustral segments are not permanent structures, however, and thus they can be smoothed out to permit propulsion of the colonic contents.

As one moves into the sigmoid colon and rectum, the intestine becomes completely enveloped by longitudinal muscle that is important to the specialized functions of this region, which include serving predominantly as a conduit and participating in defecation. The lumen of the rectum is also partially occluded by transverse folds, again formed by muscular contraction, which act as shelves to retard the passage of fecal material (Figure 9–1). Finally, the most distal portion of the gastrointestinal tract, the anal canal, is a specialized region that contains both smooth and striated muscle in its walls. In this respect, it can be compared with the most proximal gut segment, the esophagus, which is the only other segment of the gastrointestinal system whose motility is governed by both muscle types.

4 Main Phases of Gastric Secretion | Digestive System | Human | Biology

Gastric secretion has divided into four phases: 1. Nervous Phase 2. Gastric Phase 3. Intestinal Phase 4. Interdigestive Phase.

1. Nervous Phase:

A pouch of Pavlov is prepared in a dog and upon the same animal oesophagus is divided, as done in the experiment of sham feeding. The food, swallowed by the animal, comes out through the cut end of the oesophagus and does not enter stomach. In spite of it, it is found that the stomach secretes after a latent period, of about 5-10 minutes and continues for as long as 1 1/2 hours. When the vagi are cut this secretion fails to occur.

i. Stimulation of the vagus produces a secretion rich in pepsin and HCl also some mucus, the most powerful action is possibly on acid secretion. The gastric cells are stimulated by acetylcholine released after vagal action. There is also a possibility that increased amount of histamine, liberated at the mucosa of stomach after vagal stimulation, stimulates the parietal cells.

Vagal stimulation also causes vasodilatation of the gastric mucosa. Under certain conditions vagal stimulation can also stop or diminish gastric secretions. Stimulation of the vagus also increases the release of gastrin and augments the response of the cells of stomach to other type of stimuli.

ii. Stimulation of the sympathetic nerves, supplying the stomach causes vasoconstriction, but its effects on gastric secretion are not constant.

iii. Hypothalamus exerts undoubted influence upon gastric secretion. Stimulation of hypothalamus increases gastric secretion by augmenting vagal activity. Hypoglycaemia has similar effect mediated in an identical way. Experimental lesions of hypothalamus have been found to produce gastric haemorrhages, erosions and even perforations. It is believed that some such lesion may be associated with the causation of gastric ulcer.

iv. These show that the initial phase of gastric secretion is a reflex process and this type of secretion is called appetite juice by Pavlov.

On further analysis it is seen that two types of reflexes are involved in it:

i. Unconditioned Reflex:

The sensory stimulus for the unconditioned reflex arises in the mouth during chewing and swallowing of the food. The sensory nerves are the fifth, seventh and ninth cranial nerves. The motor nerve is the vagus.

ii. Conditioned Reflex (Psychic Reflex):

The existence of conditioned reflex is proved by the fact that sight or smell of the accustomed food stimulates gastric secretion. Various other conditioned stimuli can be established which can arouse gastric secretion even when no food is actually given to the dog, i.e., without the contact of food in the mouth. The sensory nerves are those of special senses, viz., vision, smell and hearing. Motor nerve is the vagus.

It has got the following characters:

i. It is rich in pepsin, acid in reaction and contains mucus.

ii. The composition of appetite juice is constant and does not vary with the type of food.

iii. The quantity varies with the intensity of appetite.

iv. The secretion of psychic juice may be inhibited by shock, fear, anxiety, etc.

v. In animals it forms a considerable part of the total gastric secretion but in man the quantity is probably much less and is not essential.

vi. Its importance lies in the fact that it helps to initiate the second phase of gastric secretion.

2. Gastric Phase (Hormonal):

At the end of sham feeding, gastric secretion elicited by cephalic phase dies away. But if food enters the stomach, further secretion of gastric juice takes place. The gastric phase of secretion is mediated by local and vagal reflex response to distention and also by the hormone gastrin released by the mucosa of the pyloric area.

Thus when the stomach is completely denervated, this secretion is not affected. This proves that this secretion is addition to a nervous reflex and mechanical irritation of food on the gastric mucosa is due to a chemical stimulus. By further experiments it has been proved that a chemical excitant is actually operating in this phase and is called gastrin (Fig. 9.33).

The following experimental facts can be put forth to uphold the gastrin theory:

i. Acid extract of pyloric mucosa, on injection, stimulates gastric secretion.

ii. At the height of gastric secretion, a substance is found to be present in the venous blood of stomach which can excite gastric secretion.

iii. Ivy and Farrell cut out a small pouch from the body of the stomach and grafted it in the mammary region of a pig. The mammary gland being highly vascular, the graft easily sets there. The wound in the stomach is adequately sutured. With such a preparation it is seen that, when the second phase of gastric secretion, is taking place in the main stomach, the grafted pouch also secretes gastric juice.

Since there is no nervous connection between the stomach and the grafted pouch and there is no separate nervous connection (vagus motor) of the pouch, secretion in the latter must be due to a chemical excitant which is carried to the pouch through blood stream.

iv. Komarov has isolated a protein derivative from the pyloric mucosa possessing strong stimulating effect on gastric secretion.

v. After resection of the pyloric part of stomach this phase of gastric secretion is greatly reduced.

vi. When coagulated egg albumin, raw meat, undigested starch or fat, is introduced into the stomach through the gastric fistula or through the oesophagotomy wound of a sleeping dog (to avoid secretion of psychic juice) no secretion takes place.

This proves that these substances neither have any mechanical effect nor carry the necessary chemical stimulus. But when meat extracts, liver extracts and partly digested meat, egg-white, etc., be introduced in the stomach, gastric secretion is stimulated. It has been demonstrated that stimulation of the vagus causes release of gastrin. This gastro-intestinal hormone is also liberated through a local reflex mechanism mediated through cholinergic nerves other than the vagus.

From these observations it can be concluded that gastrin is manufactured by the pyloric mucosa from some products of protein digestion. This substance enters the blood stream, brought back to the gastric glands and stimulates their secretion.

Nature and Action of Gastrin:

It is polypeptide in nature, two gastrins, gastrin I and II, differing in amino acid sequence have been isolated. Both of them stimulate gastric secretion.

(a) Gastrin stimulates gastric secretion—which is rich in acid but poor in pepsin,

(b) it stimulates bile secretion, and

(c) It also stimulates pancreatic secretion to a slight extent.

The gastric phase of secretion constitutes the main part of gastric juice and continues for about three hours. Unlike psychic juice, this part of secretion and varies in quality and quantity according to the type of foodstuff.

The variations are as follows:

Response to Food:

i. Meat increases both the quantity and the HCl content.

ii. Bread stimulates a secretion having the greatest digestive power.

iii. Fat inhibits secretion both in quality and quantity. [It also inhibits the movements of stomach] This depressing effect may be due to a chemical substance called enterogastrone. [see below.] The inhibitory effects of fats are more strongly exerted from the duodenum than from the stomach.

iv. Water, tea, coffee, spices, condiments, vegetable juices, etc., stimulate gastric secretion.

v. Mechanical distention of stomach by gas, such as with aerated waters, stimulates gastric secretion (and movements).

3. Intestinal Phase:

It was observed that the presence of certain food substance in the small intestine excites gastric secretion. The latent period is 2 – 3 hours but continues for 8 -10 hours. When water, meat extract, peptone and partly digested proteins etc., enter the duodenum in the process of digestion or are directly introduced into the duodenum (through a duodenal fistula), this secretion occurs.

When these parts are completely denervated this phase of gastric secretion is not affected. This proves that it is due to a chemical stimulant, a hormone or secretagogue absorbed with the food from the intestine, the exact nature of the stimulus is not known.

Gastric secretion can also be inhibited by the presence of certain substances in the duodenum.

(a) Introduction of alkali directly into duodenum inhibits gastric secretion, and

(b) Presence of fats in the duodenum inhibits gastric secretion (both the gastric and intestinal phases).

This inhibitory action of fat is due to the liberation of an intestinal hormone called enterogastrone. It inhibits gastric secretion and gastric motility. Such an inhibitory agent has been detected in the blood of fat-fed animals and has been extracted from the intestinal mucosa.

Urogastrone is another inhibitory substance similar to, but not identical with enterogastrone. It has been isolated both from the urine of a normal male and from that of a pregnant women. It exerts a specific inhibitory effect on gastric secretion (for this reason its therapeutic use in the treatment of gastric ulcer has been recom­mended). Its role in the normal process of gastric secretion is not known.

4. Interdigestive Phase:

Hydrochloric acid secretion has been found to take place at regular intervals, even in fasted man and dog. They all act by stimulating the nucleus of the vagus.

It has been observed that both hormonal and nervous mechanisms are involved in such secretion, the latter being mediated through the vagus. Recently, it is believed that the interdigestive phase is a part of intestinal phase and partly due to spontaneous secretion of saliva.

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