Gastrin

  • OMIM: 137250
  • MGI: 104768

Gastrin or polypeptide 101 (PP 101 ) is a peptide hormone of the gastrointestinal tract and exerts - from the strongest stimulus for the production of stomach acid - in addition to other effects such as the increase in the Kardiasphinkter tone.

Structurally, it is closely related to cholecystokinin. Gastrin is formed in the G cells in the pyloric antrum of the stomach and in the duodenum and is transported from there to the blood vessels to its sites of action. Rarely, an increased gastrin production by a virilizing tumor, called a gastrinoma occur.

Molding

The three forms of gastrin differ in the length of their peptide chain:

Control of the discharge

Secretion of gastrin is stimulated by:

  • The stretching of the stomach
  • Proteins and peptides in the food
  • Stimulation of the vagus nerve and the subsequent release of GRP ( gastrin releasing peptide) and acetylcholine ( thus also through consumption of nicotine)
  • Consumption of alcohol, caffeine, not by other methylxanthines

The secretion is inhibited by:

  • VIP ( vasoactive intestinal peptide)
  • Somatostatin
  • Secretin
  • GIP ( Inhibiting gastrin peptide)
  • Neurotensin

Effect

Gastrin acts mainly on the stomach. It stimulates:

  • Smooth muscle of the stomach,
  • The production of pepsinogen ( protein degradation protein precursor) in the main cells of the stomach,
  • The hydrochloric acid production by the parietal cells (activation of PLCβ ) and
  • Histamine production ( tissue hormone here for hydrochloric acid production stimulation ) of the so-called ECL cell ( Enterochromaffin -like).

Gastrin also acts on the pancreas, there it stimulates the secretion of insulin (blood sugar -lowering agents ), glucagon (blood sugar enhancer ) and somatostatin ( gastrin and pepsin inhibitors).

Decoupled effect

In the Zollinger -Ellison syndrome is caused by multiple neuroendocrine tumors ( NET), which is then most often found in the pancreas, small intestine or the liver, produced autonomously gastrin. Through the permanent rise in level of gastrin in the blood of normally closed control loop is broken.

In gastric parietal cells respond to gastrin with increased non-physiological hyperplasia and produce increased hydrochloric acid. This in turn can lead to further damage in the gastric and small intestinal mucosa.

Human Genome Organisation Mouse Genome Informatics Entrez Ensembl UniProt National Center for Biotechnology Information Zollinger–Ellison syndrome Smooth muscle tissue Gastric mucosa
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