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)

Historically, the enterochromaffin cell was the first endocrine cell type detected in avian gut; subsequently, a number of types of such cells were distinguished on the basis of the ultrastructural features of the secretory granules. More recently, immunocytochemical procedures have revealed somatostatin-, pancreatic polypeptide (PP)-, polypeptide YY-, glucagon-, secretin-, vasoactive intestinal peptide (VIP)-, gastrin-, cholecystokinin-, neurotensin-, bombesin-, substance P-, enkephalin-, motilin-, and FMRFamide-like immunoreactivity in avian gastrointestinal endocrine cells. Most endocrine cells are located in the antrum; there are a number in the proventriculus and small intestine but few in the gizzard, cecum, and rectum. Several avian gastroenteropancreatic hormones, including glucagon, VIP, secretin, bombesin, neurotensin, and PP, have been isolated and sequenced. They resemble the equivalent mammalian peptides in terms of molecular size but differ in amino acid composition and sequence; some (e.g., VIP) differ only in minor respects, others (e.g., secretin) more radically. Gastrointestinal endocrine cells appear late in development; available data indicate that few types are recognized by either immunocytochemistry or electron microscopy before 16 days of incubation. Experimental evidence has shown that at least the majority of gut endocrine cells are of endodermal origin and are not derived from the neural crest or neuroectoderm as earlier proposed. In early embryos, the progenitors of gastrointestinal endocrine cells are more widespread than are the differentiated cells in chicks at hatching. This, along with other observations, raises the question of factors that might influence the differentiation of gut endocrine cells.
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PMID:Gastrointestinal hormones in birds: morphological, chemical, and developmental aspects. 608 44

1. The effects of secretin, glucagon, cholecystokinin-pancreozymin (CCK-PZ), gastric inhibitory peptide (GIP), vasoactive intestinal peptide (VIP), somatostatin, neurotensin and enkephalin on basal, pentagastrin- and histamine-stimulated gastric acid secretion were investigated in the conscious fistula rat. 2. Glucagon and GIP were ineffective inhibitors of basal and pentagastrin-stimulated secretion. CCK-PZ stimulated acid secretion at a low dose level but at higher doses it inhibited both pentagastrin- and histamine-induced secretions. VIP was ineffective at low doses and at high doses its action was complicated by reflux of stimulated pancreatic and intestinal secretions into the stomach. Met-enkephalin inhibited histamine- but not pentagastrin-stimulated secretion. Neurotensin inhibited the response to pentagastrin but had no effect on histamine-stimulated secretion. Secretin and somatostatin were potent inhibitors of basal and pentagastrin-stimulated acid secretion with little or no effect on the response to histamine. 3. At doses completely inhibitory to pentagastrin-stimulated secretion secretin and somatostatin did not block the mobilization of gastric mucosal histamine by pentagastrin, although somatostatin caused partial competitive inhibition at lower doses of pentagastrin. Thus secretin and somatostatin inhibited pentagastrin-induced secretion neither by blocking gastric mucosal histamine mobilization nor by abolishing the direct action of histamine on the parietal cell -- findings which are inconsistent with the proposed role of histamine as the mediator of the action of gastrin on the parietal cell.
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PMID:Effects of various gastrointestinal peptides on parietal cells and endocrine cells in the oxyntic mucosa of rat stomach. 610 65

Fifteen male Holstein X Frisian calves, weighing 65 +/- 3 kg and fed a milk replacer twice daily were fitted with a return cannula loop, chronically implanted at 10 days of age in the pancreatic duct, were used. In six successive experiments we have observed the influence of an intravenous infusion of secretin, cholecystokinin pancreozymin (CCK-PZ), vasoactive intestinal peptide (VIP), glucagon, gastrin and somatostatin on pancreatic juice flow rate, and on the excretion of proteins, calcium, inorganic phosphorus, zinc and amylase activity of pancreatic juice. In two other experiments, we have studied the interaction of secretin (or CCK-PZ) with somatostatin (SRIF). Each experiment was performed 5 h after calves feeding and no milk was given to the animals during the time of sampling. Our results indicate that the endocrine regulation of the exocrine pancreas in young calves is similar to that described in other mammals. Secretin and CCK-PZ increased significantly excretion of water, calcium, magnesium, inorganic phosphorus, zinc, proteins and amylase activity. Somatostatin and glucagon inhibited effects observed with two precedent hormones. Gastrin increased pancreatic juice flow rate but excretion of protein and amylase activity do not varied significantly. VIP showed no significant effect on pancreatic excretion of water, minerals, proteins and amylase activity. However, our animals seem to be characterized by a more intense excretion of proteins and amylase in the pancreatic juice following secretin than after CCK-PZ infusion.
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PMID:The endocrine regulation of exocrine pancreas in preruminant milk-fed calves. 610 15

The effects of pirenzepine on the plasma concentrations of gut hormones in the fasting and postprandial states were studied in six healthy subjects. On separate days and in random order, 10 mg pirenzepine, in 2 ml of solvent, or 2 ml saline (0.15 mol/l) were given intravenously 30 min before a standard normal breakfast (2220 kJ). Pirenzepine was not found to affect basal or postprandial levels of insulin, glucagon, gastric inhibitory peptide (GIP), neurotensin, vasoactive intestinal peptide (VIP) or somatostatin. The basal concentration of pancreatic polypeptide (PP) was lowered (p less than 0.05) and the postprandial elevation reduced, though not significantly. While the basal concentration of motilin was also suppressed (p less than 0.05), the postprandial elevation remained unchanged following pirenzepine. The release of enteroglucagon was reduced significantly in the basal and postprandial states (p less than 0.05 and p less than 0.025 respectively). The postprandial gastrin response was prolonged slightly, but insignificantly, by pirenzepine. It is concluded that pirenzepine does not exert any major or unexpected actions on the hormonal control of digestion.
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PMID:The effect of pirenzepine on meal-stimulated gastrointestinal hormones. 611 82

Preliminary observations have indicated the existence of characteristic spectra of gastroenteropancreatic (GEP) neurohormonal peptides in endocrine tumors arising in foregut, midgut, and hindgut derivatives. In order to further explore this feature of GEP endocrine neoplasms, islet cell tumors from 14 patients were studied, as were endocrine tumors of the stomach, duodenum, and upper jejunum from 6, 5, and 2 patients, respectively. All tumors were examined immunohistochemically with antisera raised against islet hormones [insulin, somatostatin, glucagon, pancreatic polypeptide (PP)], peptides of the gastrin family [gastrin, cholecystokinin (CCK)], peptides of the secretin family [secretin, vasoactive intestinal peptide (VIP)], and substance P, neurotensin, leu-enkephalin, beta-endorphin, motilin, calcitonin, and ACTH. In addition, an ultrastructural investigation was made. Whenever possible, the immunohistochemical observations were correlated with the clinical manifestations and with the results of radioimmunochemical determination of GEP neurohormones in the blood. The pattern of immunoreactive neurohormonal peptides and the clinical picture were those to be expected in endocrine tumors arising in foregut derivatives. Some principles are proposed for the classification of GEP endocrine tumors on the basis of their histopathologic growth pattern, their spectrum of neurohormonal peptides, and their clinical manifestations.
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PMID:Neurohormonal peptides in endocrine tumors of the pancreas, stomach, and upper small intestine: I. An immunohistochemical study of 27 cases. 613 99

The distribution of vasoactive intestinal peptide (VIP), bombesin and gastrin-cholecystokinin in the chicken was studied by radioimmunoassay of tissue extracts. VIP was present in high concentrations in colon (186 +/- 29 pmol/g), cloaca (116 +/- 27 pmol/g), jejunum (97 +/- 14 pmol/g) and pancreas (15 +/- 3 pmol/g) but not detected in lung, liver or thymus. The highest concentration of bombesin was in the proventriculus (92 +/- 13 pmol/g), negligible in remaining gut but found in brain. Gel chromatography indicated two forms of bombesin: one form eluting with bombesin-14 and the other with gastrin releasing peptide. Gastrin-like immunoreactivity was found in low levels in the gut and brain. The concentrations were higher with an antiserum which cross reacted with the carboxy terminus common to gastrin-17 and CCK compared to a gastrin specific antisera (P less than 0.01). This suggests that the carboxy terminal region has been conserved during evolution. Each distribution pattern of bombesin, VIP and gastrin CCK is different, and distinct from that found in mammals, suggesting specific roles for these peptides in birds.
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PMID:Distribution of vasoactive intestinal peptide, bombesin, and gastrin-cholecystokinin like peptides in the avian intestinal tract and brain. 614 Jan 19

The effects of starvation on the tissue concentrations of some peptides common to the gastrointestinal tract and the central nervous system have been examined. Groups of 6 rats were either fed ad libitum or starved for up to 4 days and killed by decapitation. Antrum, fundus, duodenum, jejunum, ileum, colon, pancreas and brain were dissected, weighed and then frozen on dry ice. The tissues were extracted sequentially in boiling water and 3% acetic acid, centrifuged and the supernatants radioimmunoassayed for gastrin, cholecystokinin (CCK), vasoactive intestinal peptide (VIP), gastric inhibitory peptide (GIP) and somatostatin. Each peptide was not assayed in each tissue. Starvation had no effect on the concentrations of peptides measured in the fundus (somatostatin and VIP), ileum (somatostatin, GIP, VIP) and colon (somatostatin, GIP, VIP). VIP concentration was increased in the jejunum and GIP was increased in both the duodenum and jejunum. Antral gastrin was the only peptide in the gastrointestinal tract to be decreased by food deprivation. Somatostatin concentration was approximately doubled in the antrum, duodenum, jejunum and pancreas. Brain VIP was unchanged. Brain somatostatin and CCK were significantly reduced by starvation. We conclude that starvation results in organ-specific and hormone-specific alterations in tissue concentrations of peptides of the gastrointestinal tract and the central nervous system.
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PMID:Starvation in the rat: effect on peptides of the gut and brain. 614 Sep 13

This paper contains a discussion and presentation of evidence concerning vagal control of the release of some gastrointestinal peptides, the secretion of gastrin and somatostatin in particular. Some aspects of the regulation of vasoactive intestinal peptide (VIP), substance P, bombesin and insulin release by the vagus nerve are also reviewed. Data were obtained not only by electrical stimulation of the vagi but also by monitoring effects of feeding and suckling. The involvement of vagal afferents, transmitters, neurohormones in release of other hormones and humorally carried activators and inhibitors is analyzed. Particular attention is paid to the chains of reactions induced by physiological stimuli: feeding and suckling.
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PMID:Release of gastrointestinal peptides in response to vagal activation induced by electrical stimulation, feeding and suckling. 614 Dec

The use of protein A- and IgG-conjugated colloidal gold staining methods for the immuno-localisation of peptide hormones and neurotransmitters at light- and electron microscope level are described and discussed. Bright-field and dark-ground illumination modes have been used to visualise the gold-labelled antigenic sites at the light microscope level. Immunogold staining procedures at the ultrastructural level using region-specific antisera have been adopted to localise specific molecular forms of peptides including gastrin (G17 and G34), glucagon and pro-glucagon, insulin and pro-insulin, in normal tissue and in tumours of the gastroenteropancreatic system. Similar methods have been used to demonstrate the heterogeneity of p-type nerves in the enteric nervous system. Vasoactive intestinal polypeptide (VIP) has been localised to granular sites (mean +/- S.D. granule diameter = 98 +/- 19 nm) in nerve terminals of the enteric plexuses and in tumour cells of diarrhoeogenic VIP-producing neoplasias (mean +/- S.D. granule diameter = 126 +/- 37 nm) using immunogold procedures applied to ultraviolet-cured ultrathin sections. Co-localisation of amines and peptides in carotid body type I cells and in chromaffin cells of normal adrenal medulla and phaeochromocytomas has also been demonstrated. Advantages of the immunogold procedures over alternative immunocytochemical techniques are discussed.
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PMID:Immunogold staining procedure for the localisation of regulatory peptides. 618 90

The neuropeptides, substance P, vasoactive intestinal peptide (VIP), neuropeptide Y and enkephalin have been found in nerves associated with the heart and blood vessels of a range of mammals, including man. There is also evidence for some cardiovascular nerves with gastrin releasing peptide and neurotensin immunoreactivity. Substance P is in sensory nerves with a widespread distribution to the heart and all vascular beds. In general, large arteries have the densest innervation and the density of nerves decreases as arterial size decreases. In adult guinea-pigs, an adequate treatment with capsaicin causes the degeneration of almost all cardiovascular substance P nerves. Using capsaicin as a tool it has been shown that the substance P containing sensory nerves are not essential for baroreceptor reflexes. VIP nerves also have a widespread distribution, being particularly prominent in the cerebral arteries, uterine arteries and arteries of erectile and secretory tissues. Neuropeptide Y is located in the same cardiovascular nerves as noradrenaline. It is depleted from the nerves by reserpine or 6-hydroxydopamine. Enkephalin nerves have been reported with small arteries in only a few vascular beds.
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PMID:Neuropeptides contained in peripheral cardiovascular nerves. 619 37


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