Disease relevance of Gast

• However, colorectal carcinoma cells may aberrantly produce gastrin and exhibit increased expression of cholecystokinin B (CCK-B)/gastrin receptors [1].
• In the human gastrinoma culture, RC-160 inhibited gastrin release significantly more than octreotide at 10(-12)- and 10(-14)-M concentrations (P < 0.01) [2].
• We previously reported that gastrin (G17) inhibits apoptosis of AR4-2J pancreatic adenocarcinoma cells, through the activation of Akt [3].
• Serum gastrin levels are responsive to many physiologic and pharmacologic factors including hyperglycemia, somatostatin, and glucagon [4].
• RESULTS: In rats with gastric ulcer, the levels of gastrin and motilin in the antral mucosa increased, but in a lesser scale in rats with ulcer kept in high temperature than in normal temperature group, while that of somatostatin was reduced [5].

Psychiatry related information on Gast

• Effect of food deprivation on rat gastric somatostatin and gastrin release [6].
• It is concluded that partial sleep deprivation compromises gastric mucosal integrity by increasing gastric acidity, plasma levels of noradrenaline, gastrin, histamine, and decreasing gastric mucosal blood flow [7].
• The levels of circulating leptin observed after 2 and 6 h of refeeding in 18-h fast rats were significantly lowered by injection of the specific gastrin/CCK-B receptor antagonist YM022 at doses that did not affect feeding behavior [8].
• A long-term change in the level of serum gastrin, caused by dietary modification, will influence the trophic effect that gastrin has on colonic mucosa as well as on colon carcinomas [9].
• BACKGROUND: Gastrin and its analogues increase the gastric acid secretion, but also enhance mucosal defense mechanisms [10].

High impact information on Gast

• By contrast, only half of gastrin molecules are tyrosine-O-sulphated and sulphation does not influence the ability of gastrin to regulate gastric acid secretion [11].
• Although phosphorylation has received most attention, tyrosine-O-sulphation is also common and has been closely investigated in the hormones gastrin and cholecystokinin (CCK) [11].
• Moreover, the disappearance of gastrin from the pancreas during the first weeks after birth parallels the appearance of CCK in the intestine [11].
• GABA affects the release of gastrin and somatostatin from rat antral mucosa [12].
• However, immune cells in the lamina propria are the only cells that showed detectable messenger RNAs for histamine, muscarinic, gastrin, and dopamine receptors by in situ hybridization histochemistry [13].

Chemical compound and disease context of Gast

• In the present study we investigated the effects of the somatostatin (SS) analogs octreotide, RC-160, and BIM-23014 on GH release by cultured cells of human GH-secreting pituitary tumors, in normal rat anterior pituitary cells, and on gastrin release by cultured cells from a human gastrinoma [2].
• Exogenous administration of the somatostatin analogue SMS 201-995 (10 micrograms/kg) prevented both the hypergastrinemia and the increase in gastrin mRNA levels caused by omeprazole-induced achlorhydria [14].
• The inhibitory action of PYY and related peptides on gastrin-stimulated histamine release and calcium signaling was eliminated by pretreatment with 200 ng/mL pertussis toxin [15].
• E. coli LPS had a weak stimulatory effect on ECL cell BrdU uptake at 10(-6) mol/L but had no effect on gastrin-stimulated BrdU uptake [16].
• The release of gastric somatostatinlike immunoreactivity and gastrin was studied in rats with chronic achlorhydria induced by the substituted benzimidazole BY 308 [17].

Biological context of Gast

• Differential gastrin gene expression in rat gastrointestinal tract and pancreas during neonatal development [18].
• The results suggest that the mechanisms determining phosphorylation and amidation of progastrin-related peptides depend on the patterns of stimulation of gastrin cells [19].
• Pancreatic gastrin is maximally expressed during late fetal gestation before the marked rise in somatostatin, insulin, and glucagon mRNA levels which occurs during the last 4 days of gestation [18].
• Gastrin biosynthesis involves a complex series of posttranslational modifications; their elucidation requires a knowledge of the structure of the gastrin precursor [20].
• Intracellular signal transduction during gastrin-induced histamine secretion in rat gastric ECL cells [21].

Anatomical context of Gast

• Bombesin dose-dependently increased gastrin secretion; this stimulatory effect on the G cell was significantly reduced after a 72-h starvation [6].
• BACKGROUND & AIMS: In gastric antrum, somatostatin exerts a tonic inhibitory influence on gastrin and histamine secretion [22].
• Gastrin is trophic for the normal gastric oxyntic mucosa and exerts a growth-promoting action on gastrointestinal malignancy [1].
• Thus, pancreatic gastrin gene expression shows a reciprocal relationship to the developmental expression of cholecystokinin in the duodenum [18].
• SOS, either alone or co-administered with epinephrine or gastrin heptadecapeptide (G17), dose-dependently stimulated SLI release by isolated canine fundic D-cells [23].

Associations of Gast with chemical compounds

• The aim of this study was to identify the sst subtype regulating gastrin and histamine secretion in human, dog, and rat stomach [22].
• The rate of gastrin release stimulated by carbachol was suppressed significantly by each dose of somatostatin examined (10(-8) M to 10(-4) M) [24].
• Basal and acetylcholine-stimulated gastrin release were significantly lower after a 3 day starvation, whereas the inhibitory effect of acetylcholine and the stimulatory effect of glucagon on somatostatin secretion were not influenced by fasting [6].
• Feeding did not change the sulfation of amidated heptadecapeptide gastrin or its glycine-extended variant [19].
• The post-translational processing of the pancreatic gastrin peptide, however, differs in being fully tyrosine sulfated, and thus it resembles gastrin's homologue, cholecystokinin [18].

Physical interactions of Gast

• These data suggest a SS receptor/G protein uncoupling as a result of binding of pentagastrin to gastrin receptors present in pancreatic acinar cell membranes [25].
• These new compounds bear a histamine H2 receptor antagonist (H2A) pharmacophore moiety attached to a gastrin receptor antagonist (GA) pharmacophore moiety in a reversed manner, namely the head-to-head manner, different from the previously reported head-to-tail manner [26].

Regulatory relationships of Gast

• Somatostatin inhibition of basal and carbachol-stimulated gastrin release in rat antral organ culture [24].
• Indeed, we observed a coprecipitation of both kinases and an inhibition of gastrin-induced PI 3-kinase activation when JAK2 activity is blocked [27].
• Gastrin enhances gastric mucosal integrity through cyclooxygenase-2 upregulation in rats [28].
• G17 induced p38 kinase activity at doses and with kinetics similar to those observed for Akt induction [29].
• To determine whether VDCCs contribute to histamine release stimulated by gastrin or pituitary adenylate cyclase-activating polypeptide (PACAP), the presence of VDCCs and their possible modulation by peptides was investigated in a 48-h cultured rat gastric cell population containing 85% ECL cells [30].

Other interactions of Gast

• Basal antral gastrin release was inhibited by somatostatin [24].
• We demonstrated that JAK2 functions as an upstream mediator of the phosphatidylinositol 3 (PI 3)-kinase activity in gastrin signaling [27].
• Pretreatment with nifedipine (10 microM), an L-type Ca2+ channel blocker, reduced PACAP-evoked pancreastatin secretion by 50-60%, gastrin-evoked secretion by approximately 80% and abolished the response to Bay K 8644 [31].
• Evaluation of the effects of pentagastrin, gastrin and pancreatic glucagon on cell proliferation in the rat gastrointestinal tract [32].
• We examined the action of G17 (10 nM) on phosphorylation and activation of protein kinase B/Akt, a kinase known to promote cell survival [29].

Analytical, diagnostic and therapeutic context of Gast

• Gastrin and histamine were measured by radioimmunoassay [22].
• Exogenous somatostatin given by intravenous infusion to conscious rats counteracted the release of gastrin stimulated by feeding, elevated antral pH or vagal excitation [33].
• G17 also induced FOXO3 phosphorylation assessed by Western blots with anti-phospho-FOXO3 antibodies, and BAPTA-AM inhibited this effect [3].
• In the current study, the actions of synthetic (sp) and native (np) porcine and synthetic human (sh) GIP, GLP-1(7-36), and GLP-1(7-37) on SLI and gastrin secretion were compared using a gradient perfusion of peptide [34].
• Mucus, gastrin and somatostatin cells in cultured rat antral mucosa: immunofluorescence, ultrastructural and radioimmunological studies [35].

References