The Auerbach’s plexus, also known as the myenteric plexus, is a collection of ganglia that controls peristalsis and is located in the gut wall.

In the muscular layer of the wall, it is located between the circular and longitudinal muscle layers. It is a linear network of linked neurons that runs the length of the gastrointestinal system. The myenteric plexus generates an increase in gut wall tone and the strength of rhythmical contractions when stimulated.

Somatostatin-producing cells present in the pyloric antrum, duodenum, and pancreatic islets are known as D-cells or delta-cells. Somatostatin inhibits gastric acid secretion by acting directly on acid-producing parietal cells in the stomach via a G-protein coupled receptor. By suppressing the release of other hormones such as gastrin, secretin, and histamine, somatostatin can indirectly reduce stomach acid output, slowing the digesting process.
The table below summarizes the many cell types found in the stomach, as well as the substances secreted by each cell type and the function of the secretion:

Cell type/ Substance secreted/ Function of secretion
Parietal cells/ Hydrochloric acid/ Kills microbes and activates pepsinogen
Parietal cells/ Intrinsic factor/Binds to vitamin B12 and facilitates its absorption
Chief cells/ Pepsinogen/ Protein digestion
Chief cells/ Gastric lipase/ Fat digestion
G-cells/ Gastrin/ Stimulates gastric acid secretion
Enterochromaffin-like cells (ECL cells) /Histamine/ Stimulates gastric acid secretion
Mucous-neck cells/ Mucous and bicarbonate/ Protects stomach epithelium from acid
D-cells/ Somatostatin/ Inhibits gastric acid secretion

The principal enzyme involved in lipid digestion is pancreatic lipase. It breaks down triglycerides into free fatty acids and monoglycerides. Pancreatic lipase works with the help of emulsifying agents secreted by the liver and the gallbladder. The main emulsifying agents are the bile acids, cholic acid and chenodeoxycholic acid. These are conjugated with the amino acids glycine and taurine to form bile salts. Bile salts are more soluble than bile acids and act as detergents to emulsify lipids. The free fatty acids and monoglycerides form tiny particles with these bile salts called micelles. The outer region of the micelle is water-attracting (hydrophilic), whereas the inner core is water-repelling (hydrophobic). This arrangement allows the micelles to enter the aqueous layers surrounding the microvilli and free fatty acids and monoglycerides to diffuse passively into the small intestinal cells.

Pancreatic amylase breaks down some carbohydrates (notably starch) into oligosaccharides.

Chymotrypsin is a proteolytic enzyme that aids in digestion of protein

Carboxypeptidase hydrolyses the first peptide or amide bond at the carboxyl or C-terminal end of proteins and peptides

The gastric chief cells in the stomach wall releases pepsinogen. Pepsinogen is a proenzyme. It mixes with hydrochloric acid in the stomach and is converted to pepsin. Pepsin breaks down proteins into peptides aiding protein digestion.

The stomach produces gastric acid, which is a digesting fluid. The stomach secretes about 2-3 litres every day. It is involved in tissue breakdown, the conversion of pepsinogen to active pepsin, and the creation of soluble salts with calcium and iron, and has a pH range of 1.5-3.5. It also serves as an immune system by destroying microbes.

The following substances are found in gastric acid:
Water
Acid hydrochloride
Pepsinogen
mucous
Intrinsic factor

The parietal cells in the proximal 2/3 (body) of the stomach release gastric acid. The concentration of hydrogen ions in parietal cell secretions is 1-2 million times that of blood. Chloride is released against both a concentration and an electric gradient, and active transport is required for the parietal cell to produce acid.

The following is how stomach acid is secreted:

1. Gastric acid secretion is dependent on the H+/K+ ATPase (proton pump) situated in the canalicular membrane. The breakdown of water produces hydrogen ions within the parietal cell. The hydroxyl ions produced in this reaction mix quickly with carbon dioxide to generate bicarbonate ions. Carbonic anhydrase is the enzyme that catalyses this process.

2. In return for chloride, bicarbonate is carried out of the basolateral membrane. The ‘alkaline tide’ occurs when bicarbonate is released into the bloodstream, resulting in a modest rise in blood pH. The parietal cell’s intracellular pH is maintained by this procedure. Conductance channels carry chloride and potassium ions into the lumen of canaliculi.

3. Through the action of the proton pump, hydrogen ions are pushed out of the cell and into the lumen in exchange for potassium; potassium is thus efficiently recycled.

4. The canaliculi accumulate osmotically active hydrogen ions, which creates an osmotic gradient across the membrane, allowing water to diffuse outward.

Gastrin is a peptide hormone that aids in gastric motility by stimulating the generation of gastric acid by the parietal cells of the stomach. G-cells in the stomach’s pyloric antrum, the duodenum, and the pancreas release it.

The following stimuli cause the release of gastrin:

Stimulation of the vagus nerve
Hypercalcaemia
stomach bloating
Proteins that have been partially digested, particularly amino acids.
The presence of acid and somatostatin inhibits the release of gastrin.
Gastrin’s main actions are as follows:
Gastric parietal cells are stimulated to release hydrochloric acid.
ECL cells are stimulated to produce histamine.
Gastric parietal cell maturation and fundal growth stimulation
Causes the secretion of pepsinogen by the gastric chief cells.
Improves antral muscle mobility
stimulates gastric contractions
Increases gastric emptying rate and stimulates pancreatic secretion
Gallbladder emptying is induced.

Enterochromaffin-like cells (ECL cells) are a type of neuroendocrine cell located beneath the epithelium in the stomach glands. They’re most typically located near the parietal cells of the stomach. The ECL cells’ primary role is to produce histamine, which stimulates the formation of stomach acid by the parietal cells.

The table below summarizes the many cell types found in the stomach, as well as the substances secreted by each cell type and the function of the secretion:

Cell type/ Substance secreted/ Function of secretion
Parietal cells/ Hydrochloric acid/ Kills microbes and activates pepsinogen
Parietal cells/ Intrinsic factor/Binds to vitamin B12 and facilitates its absorption
Chief cells/ Pepsinogen/ Protein digestion
Chief cells/ Gastric lipase/ Fat digestion
G-cells/ Gastrin/ Stimulates gastric acid secretion
Enterochromaffin-like cells (ECL cells) /Histamine/ Stimulates gastric acid secretion
Mucous-neck cells/ Mucous and bicarbonate/ Protects stomach epithelium from acid
D-cells/ Somatostatin/ Inhibits gastric acid secretion

Achlorhydria is an autoimmune illness of the gastric parietal cells that causes insufficient stomach acid production. The parietal cells that have been injured are unable to create the necessary amount of stomach acid. As a result, the pH of the stomach rises, food digestion suffers, and the risk of gastroenteritis rises.

The secretion of hydrochloric acid and intrinsic factor is controlled by the gastric parietal cells, which are epithelial cells in the stomach. These cells can be found in the gastric glands, the fundus lining, and the stomach body.

In response to the following three stimuli, the stomach parietal cells release hydrochloric acid:

H2 Histamine receptors are stimulated by histamine (most significant contribution)
Acetylcholine stimulates M3 Receptors via parasympathetic action.
CCK2 receptors are stimulated by Gastrin.

Intrinsic factor, which is essential for vitamin B12 absorption, is also produced by stomach parietal cells.
Omeprazole is a proton pump inhibitor that is both selective and irreversible. It inhibits the H+/K+-ATPase system present on the secretory membrane of gastric parietal cells, which lowers stomach acid secretion.
Ranitidine inhibits histamine H2-receptors in a competitive manner. The reversible inhibition of H2-receptors in gastric parietal cells reduces both the volume and concentration of gastric acid.

Gastric lipase, commonly known as LIPF, is an acidic lipase released by gastric chief cells, which are found deep within the stomach lining’s mucosal layer. It’s an enzymatic protein that’s in charge of fat digestion in the stomach.

Somatostatin-producing cells present in the pyloric antrum, duodenum, and pancreatic islets are known as D-cells or delta-cells. Somatostatin inhibits gastric acid secretion by acting directly on acid-producing parietal cells in the stomach via a G-protein coupled receptor.

Somatostatin affects hormones in the following ways:
Inhibits the anterior pituitary’s secretion of growth hormone.
Inhibits the anterior pituitary’s secretion of thyroid-stimulating hormone.

The secretion of various gastrointestinal hormones is inhibited (including gastrin, CCK, secretin, motilin, VIP and GIP)

Reduces the rate at which the stomach empties.
Inhibits the release of insulin and glucagon from the pancreas.

The pancreas’ exocrine secretory activity is inhibited.
Somatostatin can also slow the digestive process by suppressing the production of hormones such gastrin, secretin, and histamine, which reduces gastric acid secretion.

A somatostatinoma is a cancerous tumour of the endocrine pancreas’ D-cells, which make somatostatin. Somatostatin inhibits pancreatic and gastrointestinal hormones when levels are high. The following clinical characteristics are related with somatostatinomas:

Insulin secretion blockage causes diabetes mellitus.
Gallstones by inhibition of CCK and secretin Steatorrhoea via inhibition of CCK and secretin

Hypochlorhydria is caused by the suppression of gastrin, a hormone that increases gastric acid output regularly.