Gastrin is a hormone that stimulates secretion of gastric acid (HCl) by the parietal cells of the stomach and stimulates gastric motility. It is released by G cells in the stomach, duodenum, and the pancreas.
Gastric secretion. 2007
- Gastrin, histamine, acetylcholine, and ghrelin stimulate whereas somatostatin, cholecystokinin, atrial natriuretic peptide, and nitric oxide inhibit acid secretion.
CHEMICAL STRUCTURE AND IMAGES
When relevant for the function
- Primary structure
- Secondary structure
- Tertiary structure
- Quaternary structure
Protein Aminoacids Percentage
The Protein Aminoacids Percentage gives useful information on the local environment and the metabolic status of the cell (starvation, lack of essential AA, hypoxia)
Protein Aminoacids Percentage (Width 700 px)
SOMATOSTATIN HAS NO HISTIDINE (depleted by former histamine synthesis?)
Low Tyrosine and Proline (low NADPH because of 1) high DNA synthesis 2) low glucose supply)
SYNTHESIS AND TURNOVER
Gastrin stimulates the stomach mucosa to produce and secrete hydrochloric acid and the pancreas to secrete its digestive enzymes. It also stimulates smooth muscle contraction and increases blood circulation and water secretion in the stomach and intestine.
- Cell signaling and Ligand transport
- Structural proteins
The vagus regulates histamine mobilization from rat stomach ECL cells by controlling their sensitivity to gastrin. 2005
Vagal excitation by hypoglycaemia (insulin) or pylorus ligation did not mobilize either gastrin or histamine. The histamine response to food was almost abolished by gastrin receptor blockade, and it was halved on the denervated side after unilateral subdiaphragmatic vagotomy.
Somatostatin and serum gastrin in normal subjects and in patients with pernicious anaemia, chronic liver and renal disease. 1975
- The effects of somatostatin (growth hormone release inhibiting hormone) on basal gastrin were studied in patients suffering from pernicious anaemia and chronic renal and liver disease, and during sequential arginine/insulin-stimulated gastrin release in normal subjects. When basal gastrin concentrations were normal (10-50 pg/ml) in controls and in patients who were in renal and liver failure, somatostatin had no effect on gastrin levels. Raised basal gastrin levels in pernicious anaemia and in 2 cases of chronic renal disease, were significantly inhibited by somatostatin with a half-life (T 1/2) of 3-4 minutes. Arginine infusion caused an insignificant rise in serum gastrin which was unaffected by somatostatin, whereas insulin hypoglycaemia significantly stimulated gastrin release, which was inhibited by somatostatin.
A HIF-1alpha-related gene involved in cell protection from hypoxia by suppression of mitochondrial function. 2008