Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01350 (gastrin)
 9,683 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The indirect immunofluorescence technique was used to demonstrate a substance reacting with gastrin antisera in the brain of Xenopus laevis. Immunoreactive material was found in two sites: (1) In the caudal hypothalamus more precisely in the nucleus infundibularis ventralis, (NIV) of the pars ventralis of the tuber cinereum, (PVTC). The fluorescent axons of the reactive parikarya of the NIV give rise to two symmetrical tracts which run rostro-ventrally and join, in the infundibular floor, the preoptico-hypophysial tract, where they form an uneven median tract coursing caudally and running along the medio-tuberal area before entering the external zone of the median eminence. (2) In the anterior preoptic area (APOA), where numerous nerve fibers and endings form a dense network near the preoptic recess. The exact origin of these terminals has not yet been determined. Control of immunohistochemical specificity shows that the labeling by gastrin antisera is suppressed by gastrin (2--17), but also by cholecystokinin (CCK) and pentagastrin (Peptavlon). These results indicate that the immunoreactive substance revealed belongs to the gastrin group and has an antigenic determinant composed of the amino acid sequence or a protion thereof common to gastrin, CCK and Peptavlon (Trp-Met-Asp-Phe). It should be emphasized that, in the brain of Xenopus laevis, both gastrin-immunoreactive sites correspond to the sites of uptake of steroid hormones (Kelley et al., 1975; Morrell et al., 1975).
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PMID:Immunohistochemical localization of a gastrin-like peptide in the brain of an amphibian, Xenopus laevis Daud. 38 28

The gastric acid secretion was studied in 17 extremely obese patients after injection of synthetic gastrin (Peptavlon). The mean basal acid output (BAO) and the peak acid output (PAO) were both within normal range. Positive correlation was found between PAO and body weight. Gastric banding was performed as treatment of the obesity, and the gastric acid secretion was studied in the proximal and the distal pouch after a mean postoperative interval of 8 (range 4-20) weeks. BAO was similar after banding, but PAO was significantly decreased (from 26.3 +/- 3.6 to 16.2 +/- 2.2 mmol/h). PAO and BAO were almost identical in the two pouches, despite great difference in their size.
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PMID:Gastric acid secretion in extremely obese subjects before and after gastric banding. 361 62

1. Gastric mucosal blood flow (MBF) and gastric acid secretion have been compared and related during the infusion of a wide dose range of gastrin extracts, pentapeptide (Peptavlon, I.C.I. 50123) and histamine.2. Constancy of increase in mucosal blood flow relative to H(+) secretion was obtained with gastrin stimulation, whereas histamine stimulation produced higher ratios of mucosal blood flow to H(+) secretion, and these ratios declined as each experiment continued.3. The importance of considering only the increase in mucosal blood flow in relation to acid secreted is demonstrated.4. It is concluded that the differences shown in the DeltaMBF/DeltaH(+) with histamine and gastrin stimulation provide further evidence that the amidopyrine clearance technique measures gastric mucosal blood flow.
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PMID:Mechanisms relating gastric acid secretion and mucosal blood flow during gastrin and histamine stimulation. 515 93

After a meal the serum concentrations of the N-terminal tridecapeptide-like fragment of gastrin-17, (1-13)G-17, increased markedly in patients with active duodenal ulcer, but less so in healthy subjects. Consequently the synthetic (1-13)G-17 was infused intravenously in doses that resulted in concentrations similar to those measured in duodenal ulcer patients in order to examine whether the N-terminal fragment influences gastric acid secretion. Doses of 125 and 400 pmol (1-13)G-17/kg per h inhibited the meal-stimulated acid secretion by 36% (P less than 0.05) and 66% (P less than 0.05) respectively. The release of endogenous C-terminal gastrin immunoreactivity was not influenced. The infusion of (1-13)G-17 also inhibited the acid response to exogenous gastrin-34, gastrin-17 and Peptavlon, but not to gastrin-4. The results suggest that the N-terminal gastrin-17 fragment--although devoid of the hitherto considered only active site of gastrin--plays a significant role in the regulation of the gastric acid secretion in patients with active duodenal ulcer.
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PMID:The N-terminal tridecapeptide fragment of gastrin-17 inhibits gastric acid secretion. 666 38