Disease relevance of GAS

• Instillation of liver extract into the HP stimulated acid secretion from the HP but caused no change in serum gastrin and no change in acid secretion from the gastric fistula [1].
• Group-2 calves had increased plasma pepsinogen and gastrin values and decreased weight gains, and total serum protein and albumin concentrations from the 2nd week of infection onward [2].
• The rise in blood gastrin levels may also be partly responsible for the marked hyperplasia of the fundic mucosa seen in abomasal infections [3].
• Differences in the course of gastrin and pepsinogen late in the grazing season can be correlated with larval inhibition and the possibility of ostertagiasis Type II [4].
• During clinical outbreaks mean gastrin levels frequently reached 1,000 pg/ml with a severe weight loss and a mean pepsinogen level of 5,000 mU tyr [5].

High impact information on GAS

• We report here that dietary components coming in contact only with oxyntic gland mucosa stimulate near maximal acid secretion through a local, H-sensitive mechanism that does not involve gastrin [1].
• Gastrin concentration in the medium decreased with time in culture until no hormone was detected between 2 and 6 weeks, possibly because of endocrine cell dedifferentiation and an increased proportion of fibroblasts in the population [6].
• Gastrin induced translocation of PKCalpha from cholangiocyte cytoskeleton to membrane [7].
• Gastrin inhibits cholangiocyte growth in bile duct-ligated rats by interaction with cholecystokinin-B/Gastrin receptors via D-myo-inositol 1,4,5-triphosphate-, Ca(2+)-, and protein kinase C alpha-dependent mechanisms [7].
• We concluded that gastrin inhibits cholangiocyte growth in BDL rats by interacting with CCK-B/gastrin receptors through a signal transduction pathway involving IP(3), Ca(2+), and PKCalpha [7].

Chemical compound and disease context of GAS

• The effect of a selective beta 2-adrenoceptor agonist on basal volume and on insulin-, 2-deoxy-D-glucose (2-DG)-, and food-induced gastrin release was studied in conscious gastric fistula dogs [8].

Biological context of GAS

• In order to deduce the primary structure of bovine preprogastrin we therefore sequenced a gastrin DNA clone isolated from a bovine liver cosmid library [9].
• Bovine and feline gastrin cDNA sequences and the amino acid and nucleotide sequence homologies among mammalian species [10].
• 6. The results indicate that the chemical stimulation of the oxyntic gland area by peptic digests is capable of inducing acid secretion by a local, gastrin-independent, partially neural reflex mechanism; sensitive to pH, pressure and secretin [11].
• 3. This dose of neurotensin produced no significant change in mean heart rate, aortic blood pressure, plasma gastrin or glucose concentration [12].
• Neither peptide produced a discernible change in mean heart rate or aortic blood pressure, or in the mean arterial plasma concentrations of enteroglucagon, gastric inhibitory peptide (GIP), gastrin or cholecystokinin (CCK) [13].

Anatomical context of GAS

• We studied the role of gastrin in regulating cholangiocyte proliferation induced by bile duct ligation (BDL) [7].
• 2. Liver extract meal kept in the stomach at pH 5.5 (by intragastric titration) produced a marked increase in gastric acid and pancreatic protein secretion accompanied by a rise in serum gastrin and pancreatic polypeptide levels [14].
• 3. An 11-fold increase in gastrin mRNA expression was recorded in the parasitized animals which was accompanied by a 23.8% reduction in pyloric mucosal gastrin content and an apparent drop of 24.7% in the number of gastrin-producing G cells detected [15].
• Differential expression of A- and B-subtypes of cholecystokinin/gastrin receptors in the developing calf pancreas [16].
• 3. In dogs release of pancreatic glucagon in response to splanchnic nerve stimulation was not suppressed by atropine (0.2 mg/kg) or somatostatin, at a dose that caused a steady fall in the concentration of gastrin in the circulating plasma (0.5 microgram-kg-1 min-1) [17].

Associations of GAS with chemical compounds

• The cleavage following a pair of lysine residues yields gastrin 17 [10].
• We found that pairs of arginine residues flanking gastrin 34, the typical processing site sequence of all other preprogastrins and many peptide hormones, were arginines in the bovine preprogastrin, but the first basic amino acid pair had changed to Arg-Trp (57-58 residues) instead of Arg-Arg in the feline preprogastrin [10].
• The gastrin mRNA of each animal encodes a preprogastrin of 104 amino acids consisting of a signal peptide, a prosegment of 37 amino acids, and a gastrin 34 sequence, followed by a glycine (the amide donor) [10].
• Gastrin effects on cholangiocyte functions were blocked by L-365,260, BAPTA/AM, H7, and staurosporin but not by L-364,718 [7].
• To evaluate if gastrin effects on cholangiocyte proliferation are mediated by the isoform PKCalpha, we evaluated (1) for the presence of PKCalpha in cholangiocytes and (2) the effect of gastrin on the PKCalpha protein expression in a triton-soluble (containing cytoplasm + membrane) and a triton-insoluble (containing cytoskeleton) fraction [7].

Other interactions of GAS

• Exogenous bovine pancreatic polypeptide caused little change in gastric secretion and serum gastrin but resulted in a profound suppression of pancreatic secretion [14].
• 2. Under these conditions ingestion of milk was followed by a prompt rise in the concentrations of pancreatic glucagon, PP and gastrin in the arterial plasma but the usual rises in plasma glucose and insulin concentration were absent [18].
• Secretin (10 (-7) M) caused a 4- to 6-fold increase in cAMP accumulation, while glucagon, vasoactive intestinal peptide, and gastrin caused little if any stimulation [19].
• Fecal consistency was significantly higher during wk 1 of life, and gastrin and glucose-dependent insulinotropic polypeptide increased only on d 1 and/or 2 of life in calves already fed colostrum on d 1, expressing improved functioning of the gastrointestinal tract [20].
• 5-HT-immunoreactive cells were most numerous, somatostatin-, gastrin-, motilin- and BPP-immunoreactive cells were moderately numerous, whereas CCK-immunoreactive cells were rare [21].

Analytical, diagnostic and therapeutic context of GAS

• Total abdominal vagotomy did not alter gastrin secretion but further inhibited acid output in response to the test meal [22].
• Blood samples were drawn from a chronic jugular vein catheter and gastrin, and somatostatin were determined by radioimmunoassay [23].
• The regulation of gastrin release in rodent antral mucosal organ cultures was investigated [24].
• Pyloric mucosal total gastrin concentrations remained unaltered in the infected calves until day 28 when levels fell to 36.9 per cent of control group values (P < 0.01) [25].
• Calves infected by surgical transplantation of adult Ostertagia ostertagi had raised levels of plasma pepsinogen and those in which the largest number of worms established also had elevated plasma gastrin concentrations [26].

References