Question

1. A patient has a tumor causing them to secrete excess gastrin all of the time, regardless of the levels of its normal stimuli. How will the following compare to that of a normal patient? Will they be lower, higher, or the same? For each one, explain your answer.

   1. Level of gastric pepsin

   2. Gastric pH

   3. Histamine secretion from ECL cells

   4. Gastric motility (movement of partially digested chyme into small intestine)

   5. Plasma CCK levels

Answer 1

Gastrin is synthesized in G cells, which are located in gastric pits, primarily in the antrum region of the stomach. In general, the primary stimulus for secretion of gastrin is the presence of certain foodstuffs, especially peptides, certain amino acids and calcium, in the gastric lumen.

Gastrinomas may occur as single tumors or as multiple small tumors. A gastrinoma (Zollinger-Ellison syndrome) is a neuroendocrine tumor that secretes a hormone called gastrin. Too much gastrin in the blood (hypergastrinemia) results in the overproduction of gastric acid by parietal cells in the stomach.

Level of gastric pepsin (INCREASES)

Gastrin and vagus nerve trigger the release of both pepsinogen and HCl from the stomach lining when food is ingested. HCl creates an acidic environment, which allows pepsinogen (inactive) to unfold and cleave itself and thereby generating pepsin (the active form).

Gastric pH (INCREASES)

Gastrin receptors are found on parietal cells, and binding of gastrin, along with histamine and acetylcholine, leads to fully-stimulated acid secretion by those cells. So gastric pH is acidic (low) in nature. Gastrin works on the parietal cells of the gastric glands, causing them to secrete more hydrogen ions into the stomach lumen. In addition, gastrin acts as a trophic factor for parietal cells, causing parietal cell hyperplasia. Thus, there is an increase in the number of acid-secreting cells, and each of these cells produces acid at a higher rate.

Histamine secretion from ECL cells (INCREASES)

Enterochromaffin like (ECL) cells bear gastrin receptors, and this cell may be the most important target of gastrin with regard to regulating acid secretion. Stimulation of ECL cells by gastrin leads to histamine release, and histamine binding to H2 receptors on parietal cells is necessary for full-blown acid secretion.

Gastric motility (movement of partially digested chyme into small intestine) (INCREASES)

gastrin receptors have been observed on certain gastric smooth muscle cells which supports the role of gastrin in regulating gastric motility.

Plasma CCK levels (INCREASES)

In addition to above cell targets, gastrin also stimulates pancreatic acinar cells via binding to cholecystokinin receptors. Though CCK increases but there is significant inactivation of pancreatic enzymes