Digestion in the Stomach

Digestion in the stomach occurs through mechanical means, i.e., grinding and churning of food, and by chemical means, in which HCL and pepsin break down proteins. Our stomachs secrete about 3L of gastric juice per day, which has several roles:

• Acids in the juice initiate protein digestion (and some fat digestion) and kill microorganisms.
• Gastric juices facilitate the absorption of iron, calcium, vitamin B12, thyroid hormone, and some drugs.
• Thick, bicarbonate-rich mucous secretions protect the stomach lining from acids.

Three phases of gastric juice secretion: The cephalic phase is initiated by the sight, smell, thought, or taste of food, and by swallowing; about 1/3rd of gastric juices is secreted during this phase. The gastric phase is initiated by stomach distention, the presence of proteins and caffeine, and by rising pH; about 2/3 of gastric juices are secreted during this phase. The intestinal phase is a short phase initiated by the presence of food in the duodenum; only a small proportion of gastric juices are secreted in this phase. Oxyntic glands are found in the body of the stomach, and contain chief and parietal cells. Pyloric glands are found in the stomach antrum; they contain mucous cells and G-cells. Mucous cells secrete mucus, which is rich in bicarbonate and helps to neutralize stomach acids. Chief cells secrete pepsinogen, which is a proenzyme of pepsin. Parietal cells secrete HCL and intrinsic factor. HCL has several roles:

• It lowers stomach pH, which activates pepsinogen to form pepsin, the enzyme that aids in protein digestion.

Once activated, pepsin can autoactivate pepsinogen, forming even more pepsin.

• HCL also denatures proteins, which makes it easier for pepsin to digest them.

• HCL kills microorganisms that arrived with ingested foods.

Intrinsic factor facilitates vitamin B12 absorption n the ileum of the small intestine. The following stimulate parietal cell release of HCL:

• Histamine, which is released by Enterochromaffin-like cells.
• Gastrin, which is secreted by G cells (gastrin-secreting cells) and travels in the systemic circulation.
• Acetylcholine, which is released by the vagus nerve.

Potentiation: In addition to their independent effects, histamine, gastrin, and acetylcholine interact to produce combined response greater than their sums – this is called potentiation. These interactions are important when we consider drugs that inhibit HCL secretion later in this tutorial. Return to the G cells and show that the following stimulate gastrin release:

• The presence of amino acids.
• Vagus nerve release of Gastrin-Releasing Peptide (GRP).
• Stomach distention, acting through local responses, leads to enteric acetylcholine release.

When chyme has moved to the small intestine and HCL secretion is no longer needed, D cells release somatostatin. Somatostatin acts directly on parietal cells and indirectly, via histamine and gastrin release, to block HCL secretion. Gastritis is inflammation of the stomach, and occurs when the mucosal and epithelial barriers of the stomach fail. To inhibit HCL secretion, we might recommend H2 blockers, such as Cimetidine, which blocks the actions of histamine on parietal cells. We might also try muscarinic blockers, such as Atropine, to block the stimulatory effects of acetylcholine. Note that both histamine and muscarinic blockers inhibit the potentiation effects of their targets, leading to a greater than expected reduction in HCL. On the other hand, proton-pump inhibitors, such as Omeprazole, block the Hydrogen/Potassium pump necessary for acid production. More on: Gastric and duodenal ulcers Zollinger-Ellison Syndrome