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

The present experiments have been carried out in order to establish whether the stimulatory effect of bombesin on the chicken gastric acid secretion is a direct effect or is mediated by the release of hormones, such as the Avian Pancreatic Petide and/or Gastrin. removal of the pancreas, which is known to be the site of starage of the Avian Pancreatic Polypeptide, does not produce any decrease of the stimulant effect of bombesin on gastric secretion. Removal of the zone between the gizzard and duodenum, which shows histological features similar to those of the mammalian antrum and in which gastrin cells have been described, sharply decreases the basal values of gastric secretion as well as the stimulant effect of bombesin, while the effectiveness of caerulein, a gastrin-like peptide directly acting on oxintopeptic cells, is maintained. In chickens deprived of the duodenum-gizzard zone, bombesin shows a stimulant effect on pancreatic secretion indistinguishable from that observed in intact animals. It is concluded that the gastric but not pancreatic, action of bomtesin is mediated through the release of a factor(gastrin) from the gizzard-duodenum junction. Release of Avian Pancreatic Polypeptide from the pancreas is not involved in the mechanism of the action of bombesin on gastric secretion of the chicken.
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PMID:On the mechanism of action of bombesin on gastric and pancreatic secretion of the chicken. 101 25

The influence of recombinant human interleukins-1 beta and -1 alpha and rat interleukin-1 beta on gastric acid secretion was investigated in awake rats with pylorus ligation. IC injection of either human interleukin-1 beta, human interleukin-1 alpha, or rat interleukin-1 beta induced a dose-dependent inhibition of gastric acid output. At IC doses less than 100 ng, human interleukin-1 beta was more effective than the other forms or sources of interleukin-1, whereas at higher doses (100-500 ng), human interleukins-1 beta and -1 alpha and rat interleukin-1 beta were equipotent. The inhibitory effect was observed 30 minutes after interleukin-1 injection and maintained throughout the 6-hour experimental period. IC injection of interleukin-1 beta inhibited vagally stimulated gastric acid secretion induced by IC injection of the stable thyrotropin-releasing hormone analogue RX 77368. Indomethacin (1, 5, and 10 mg/kg, IP, -30 minutes) induced a dose-related prevention of the inhibitory effect of IC interleukin-1 beta. IC injection of the corticotropin-releasing factor antagonist alpha-CRF9-41, bilateral adrenalectomy, and noradrenergic blockade with bretylium did not influence the antisecretory effect of interleukin-1. Polypeptide action was not related to changes in circulating gastrin levels. Human interleukin-1 beta injected IV also inhibited gastric acid secretion, but the peripheral dose required to induce a significant effect was 10(3)-fold higher than when given centrally. These results show that IC interleukin-1 beta acts centrally to induce a long-lasting inhibition of gastric acid secretion, and this effect requires the integrity of prostaglandin pathways. These data suggest a possible interaction between the immune and gastrointestinal systems.
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PMID:Central action of recombinant interleukin-1 to inhibit acid secretion in rats. 212 79

The distribution of polypeptide-YY cells within the gastric and duodenal mucosa of the rat and the development of their populations were examined daily from 3 days before birth until day 8 postpartum and after weaning, on day 25 postpartum, using a precise technique of quantification. Polypeptide-YY cells appeared in the stomach around the 19th day of gestation. They were always more numerous in the antral mucosa and particularly in the pyloric sphincter area than in the fundic mucosa. Immunogold staining at the electron-microscopic level revealed that, in the antrum, polypeptide-YY was colocalised with gastrin in endocrine cells mainly of type G and, more rarely, in cells of intestinal type IG. Comparison of the gastrin and polypeptide-YY cell populations in the same rats indicated that, except at day 6 postpartum, there were fewer gastric polypeptide-YY cells than immunoreactive gastrin cells and that polypeptide-YY cells were 8 times less numerous than gastrin cells at day 25 postpartum. Polypeptide-YY cells were clearly present in the duodenum of the 19-day-old embryo. This population increases with age until day 8 postpartum, then significantly decreases (by 87%) between days 8 and 25 postpartum. Because polypeptide-YY may inhibit secretion of gastric acid, it is possible that the presence of significant population of polypeptide-YY cells in the upper digestive tract during the first postnatal week of life may play a role (endocrine or paracrine) in the decreased acid secretion occurring in the newborn rat.
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PMID:Growth pattern of the polypeptide-YY cell population in the upper digestive tract of the rat during the perinatal period and after weaning. 269 33

The influence of the autonomic nervous system on the secretion of somatostatin from the antral and the fundic parts of the stomach and from the pancreas of the pig was investigated in experiments involving electrical stimulation of the vagal nerves and the splanchnic nerves in (1) intact, anesthetized pigs and (2) isolated perfused preparations of (a) antrum with intact vagal supply, (b) pancreas with intact vagal supply, (c) pancrease with intact sympathetic supply. The results clearly demonstrated that parasympathetic activity inhibits D-cell function in all gastro-pancreatic tissues; antral gastrin secretion was inversely correlated to somatostatin secretion and it is suggest that antral D-cell secretion participates in the control of gastrin secretion; the inhibitory effect of Gastric Inhibitory Polypeptide (GIP) as well as intraluminal HCl on gastrin secretion may be exerted via the stimulatory effect of both on somatostatin secretion. The sympathetic innervation of the pancreas is also clearly inhibitory to the pancreatic somatostatin secretion, whereas sympathetic nervous activity influences little the gastric somatostatin release.
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PMID:Nervous control of gastro-pancreatic somatostatin secretion in pigs. 612 87

Peptide YY (PYY) is a 36 amino acid, straight chain polypeptide, which is co-localized with GLP-1 in the L-type endocrine cells of the GI mucosa. PYY shares structural homology with neuropeptide Y (NPY) and pancreatic polypeptide (PP), and together form the Neuropeptide Y Family of Peptides, which is also called the Pancreatic Polypeptide-Fold Family of Peptides. PYY release is stimulated by intraluminal nutrients, including glucose, bile salts, lipids, short-chain fatty acids and amino acids. Regulatory peptides such as cholecystokinin (CCK), vasoactive intestinal polypeptide (VIP), gastrin and GLP-1 modulate PYY release. The proximal GI tract may also participate in the regulation of PYY release through vagal fibers. After release, dipeptidyl peptidase IV (DPP-IV; CD 26) cleaves the N-terminal tyrosine-proline residues forming PYY(3-36). PYY(1-36) represents about 60% and PYY(3-36) 40% of circulating PYY. PYY acts through Y-receptor subtypes: Y1, Y2, Y4 and Y5 in humans. PYY(1-36) shows high affinity to all four receptors while PYY(3-36) is a specific Y2 agonist. PYY inhibits many GI functions, including gastric acid secretion, gastric emptying, small bowel and colonic chloride secretion, mouth to cecum transit time, pancreatic exocrine secretion and pancreatic insulin secretion. PYY also promotes postprandial naturesis and elevates systolic and diastolic blood pressure. PYY(1-36) and PYY(3-36) cross the blood-brain barrier and participate in appetite and weight control regulation. PYY(1-36) acting through Y1- and Y5-receptors increases appetite and stimulates weight gain. PYY(3-36) acting through Y2-receptors on NPY-containing cells in the arcuate nucleus inhibits NPY release and, thereby, decreases appetite and promotes weight loss. PYY may play a primary role in the appetite suppression and weight loss observed after bariatric operations.
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PMID:Peptide YY(1-36) and peptide YY(3-36): Part I. Distribution, release and actions. 1668 37

Biochemical markers are applied in gastroenteropancreatic neuroendocrine tumours (GEP-NETs) for diagnostic, prognostic or predictive purposes. Chromogranin A is the most important general marker and it is recommended to be measured in every patient with a suspected NET, whereas Neuron Specific Enolase is elevated mainly in poorly differentiated NETs. Pancreatic Polypeptide is used in the diagnosis of pancreatic non-functioning NETs, whereas Chorionic Gonadotrophin has an adjunctive role. In the case of functioning tumours, specific markers should be sought and monitored during follow up. Endogenous hyperinsulinemia is suggested in the presence of non-suppressible insulin and proinsulin levels during hypoglycemia, whereas high fasting or stimulated gastrin levels along with elevated gastric acid output are diagnostic for the Zollinger-Ellison syndrome. Glucagon, vasoactive intestinal polypeptide (VIP) and somatostatin are markers for glucagonoma, VIP-oma and somatostatinoma syndromes respectively. In case of ectopic paraneoplastic syndrome, the relevant hormone serves as a diagnostic and prognostic marker.
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PMID:Biochemical markers for gastroenteropancreatic neuroendocrine tumours (GEP-NETs). 2358 19

Nuclear medicine plays a pivotal role in the management of patients affected by neuroendocrine neoplasms (NENs). Radiolabeled somatostatin receptor analogs are by far the most advanced radiopharmaceuticals for diagnosis and therapy (radiotheranostics) of NENs. Their clinical success emerged receptor-targeted radiolabeled peptides as an important class of radiopharmaceuticals and it paved the way for the investigation of other radioligand-receptor systems. Besides the somatostatin receptors (sstr), other receptors have also been linked to NENs and quite a number of potential radiolabeled peptides have been derived from them. The Glucagon-Like Peptide-1 Receptor (GLP-1R) is highly expressed in benign insulinomas, the Cholecystokinin 2 (CCK2)/Gastrin receptor is expressed in different NENs, in particular medullary thyroid cancer, and the Glucose-dependent Insulinotropic Polypeptide (GIP) receptor was found to be expressed in gastrointestinal and bronchial NENs, where interestingly, it is present in most of the sstr-negative and GLP-1R-negative NENs. Also in the field of sstr targeting new discoveries brought into light an alternative approach with the use of radiolabeled somatostatin receptor antagonists, instead of the clinically used agonists. The purpose of this review is to present the current status and the most innovative strategies for the diagnosis and treatment (theranostics) of neuroendocrine neoplasms using a cadre of radiolabeled regulatory peptides targeting their receptors.
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PMID:Current Status of Radiopharmaceuticals for the Theranostics of Neuroendocrine Neoplasms. 2829