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)

26 children were investigated on an average 11.5 years after partial (n = 13) and total (n = 13) colonic resection. Total colectomy was followed by an increased frequency of gastrointestinal symptoms such as recurrent abdominal pain, flatulence, attacks of diarrhoea, frequent and pasty or liquid stools with strange smell. An increased salt or fluid intake was observed in one half of these patients. Their height and bone age was slightly but significantly reduced. Laboratory investigations revealed no significant deficiencies of electrolyts, vitamins or trace elements. However Renin (mean and 2s-range = 5.2; 2.7-6.8 ng/ml.h, normal values (NV) 1.3; 0.5-4.0 ng/ml.h, p less than 0.02), aldosterone (242.1; 168.4-357.8 pg/ml, NV 78.9; 39.4-168.4 pg/ml, *p less than 0.02), conjugated bile acids (11.3; 5.2-20.0 mumol/1, NV 4.2; 1.5-7.0 mumol/1, p less than 0.01) and serum urea concentration (32.5; 20.8-48.7 mg/dl, NV 14.6; 6.0-22.5 mg/dl, p less than 0.01) were significantly elevated. Three postprandial plasma levels of gastrin, VIP and neurotensin were within normal limits. In patients with partial large bowel resection all signs were less pronounced. According to our results a special diet in children years after colectomy seems not to be required.
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PMID:[Late results following partial and total colectomy in infancy]. 328 87

A review of neuroendocrine features in breast carcinomas is presented and markers for neuroendocrine cells are discussed. Immunostaining for neuron specific enolase is the best screening marker for neuroendocrine cells in breast carcinomas, but immunoreactivity for hormones is not present in all neuron specific enolase (NSE) positive cases. Normal myoepithelial cells are also NSE positive. Thirty per cent of breast carcinomas are NSE positive. Biochemical demonstration of ACTH, PTH and calcitonin, and immunohistochemical demonstration of ACTH, bombesin, serotonin, prolactin, gastrin, VIP, leu-enkephalin, pancreatic polypeptide, beta-endorphin and sub P has been reported in breast carcinomas. Neuroendocrine cells have not been convincingly demonstrated in the normal breast or in benign breast lesions.
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PMID:Neuroendocrine differentiation in breast lesions. 329 Aug 69

There is a recognised association between pernicious anaemia and the development of gastric carcinoma, endocrine cell hyperplasia, and carcinoid tumour. Multiple endoscopic biopsies from the body mucosa of seven patients with pernicious anaemia showed small intestinal metaplasia with varying degrees of inflammation, fibrosis, and expansion of the lamina propria. Using conventional silver and lead stains, endocrine cells were inconspicuous. Staining for the general neural and neuroendocrine markers NSE and PGP 9.5 revealed a proliferation of endocrine cells in the epithelium and isolated clumps of endocrine cells in the lamina propria. The clumps were composed of two cell types, either small or large. Some of these endocrine cells showed gastrin, 5HT, VIP and substance P immunoreactivity of varying intensity. Ultrastructurally nine morphologically distinct types of granules were found some of which correlated with the immunohistochemistry. Some separate islands were composed solely of endocrine cells while others had a definite neural component, suggesting that the former arise from 'budding off' of enteroendocrine cells and the latter originate from the neuroendocrine cells of the lamina propria plexus. Thus there may be a dual origin of carcinoid tumours. Carcinoid tumours associated with pernicious anaemia tend to be multifocal and are infrequent. Less than 50 such cases have hitherto been reported. Our findings of endocrine cells proliferations in seven cases of pernicious anaemia indicate that this may be an adaptive change that occurs frequently and provides the basis on which carcinoids, less frequently, develop.
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PMID:Pernicious anaemia and mucosal endocrine cell proliferation of the non-antral stomach. 352 38

A tabular synopsis is presented for articles concerned with the effects of peptides on the central nervous system that appeared in the journal Peptides from 1980-1985. A table arranged alphabetically by peptide and one arranged by effects, both listing routes of injection, species, direction of change, and qualifying notes, provides easy cross-referencing of peptides and their effects. Over 80 peptides and over 135 effects are listed. The list of peptides includes, but is not limited to: ACTH, angiotensin, bombesin, bradykinin, calcitonin, casomorphin, CCK, ceruletide, CGRP, CRF, dermorphin, DSIP, dynorphin, endorphins, enkephalins, GRF, gastrin, LHRH, litorin, metkephamid, MIF-l, motilin, MSH, NPY, NT, oxytocin, ranatensin, sauvagine, substances P and K, somatostatin, TRH, VIP, vasopressin, and vasotocin. The list of effects includes, but is not limited to: aggression, alcohol, analgesia, attention, avoidance, behavior, cardiovascular regulation, catalepsy, conditioned behavior, convulsions, dopamine binding and metabolism, discrimination, drinking, EEG, exploration, feeding, fever, gastric secretion, GI motility, grooming, learning, locomotor behavior, mating, memory, neuronal activity, open field, operant behavior, rearing, respiration, satiety, scratching, seizure, sleep, stereotypy, temperature, thermoregulation and tolerance.
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PMID:Central nervous system effects of peptides, 1980-1985: a cross-listing of peptides and their central actions from the first six years of the journal Peptides. 353 8

Using the semi-thin/ultra-thin technique six different immunoreactive endocrine cell types are ultrastructurally identified in 0.5% glutaraldehyde fixed gut of B. conchonius. In addition two of them (gastrin- and PP-immunoreactive cells) are also characterized with the immunogold method, showing that the immunoreactivity is only restricted to the secretory granules. Size distribution histograms and the average diameters of 30% (d30) of the largest granules are given, showing a gradual increase in granule size from unspecific immunoreactive cells, (d30 = 110 nm) via gastrin- (119 nm), VIP-like- (127 nm), met-enkephalin- (143 nm) and PP- (174 nm) to glucagon-immunoreactive cells (178 nm). The presence of PP- and glucagon-immunoreactivity in the same cells and the consequence for their granule size is discussed. In the distal part of the gut endocrine cells are found showing no immunoreactivity with the antisera used; their granules (d30 = 144 nm) were, although not significantly, larger then those of VIP-like-immunoreactive cells, also found in that part of the gut. It is supposed that they represent substance P-immunoreactive cells. Unfortunately, secretory granules of several cell types showed about 20% more shrinkage in 0.5% glutaraldehyde fixed tissue, than in osmicated tissue.
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PMID:Ultrastructural characterization of 6 immunoreactive enteroendocrine cells in Barbus conchonius (Teleostei, Cyprinidae). 353 12

The role of the vagus nerve in the control of gastrin releasing peptide (GRP) stimulated gastroenteropancreatic hormone release and gastric acid secretion was investigated in four conscious gastric fistula dogs using a technique of bilateral cryogenic vagal blockade. A 90-min infusion of GRP at a dose of 400 pmol X kg-1. h-1 produced significant elevations in plasma levels of gastrin, motilin, GIP, enteroglucagon, insulin, pancreatic glucagon, pancreatic polypeptide and VIP. Vagal blockade reversibly inhibited the rise of plasma PP and significantly blunted the elevation of plasma VIP. However, the GRP stimulated response of the other hormones investigated was not modified by vagal blockade. Similarly, the substantial secretion of gastric acid observed with GRP was not influenced by vagal blockade. Thus GRP acts predominantly via mechanisms which are independent of vagal integrity, findings that are in support of a major role for the local neuromodulation of hormone release and gastric acid secretion.
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PMID:The role of vagal integrity in gastrin releasing peptide stimulated gastroenteropancreatic hormone release and gastric acid secretion. 388 1

Intestinal adaptation has been studied in rats with pancreatic atrophy induced by feeding a copper-deficient diet and penicillamine and in rats with carbohydrate maldigestion induced by feeding of an alpha-glucosidase inhibitor (acarbose). Pancreatic atrophy led to a significant increase of weight, protein, and DNA content as well as specific activities and total amounts of the enzymes sucrase and maltase in the distal but not in the proximal part of the small intestine. Plasma levels of CCK and GIP were significantly higher in rats with pancreatic atrophy, whereas plasma levels of gastrin and insulin were lower. Tissue concentrations of gastrin in the antrum and GIP in duodenum and jejunum were unchanged. Duodenal CCK and jejunal substance P, somatostatin, and VIP and ileal substance P and somatostatin were significantly decreased in rats with acinar atrophy. Glucosidase inhibition by acarbose feeding led to weight increase of the small intestine and cecum. This was more marked when acarbose was fed together with a fiber-free diet. Under these conditions the protein and DNA content also increased significantly in both gut segments and maltase and sucrase content predominantly in the distal part. Insulin plasma concentration decreased significantly in the acarbose-fed groups, whereas GIP, gastrin, and CCK plasma concentrations remained unchanged. After fiber-rich diet tissue concentrations of gastrin in the antrum and insulin in the pancreas were significantly higher and GIP concentrations in the duodenum and jejunum significantly lower than after fiber-free diet. Acarbose increased the pancreatic insulin concentration only in the fiber-free group and did not influence gastrin and GIP concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Adaptation of the small intestine to induced maldigestion in rats. Experimental pancreatic atrophy and acarbose feeding. 389 54

In the present study, a radioimmunoassay for oxytocin determinations is presented. In addition, we investigated whether the elevation of insulin, VIP and gastrin levels demonstrated to occur in response to suckling in lactating dogs may be induced by released oxytocin. Therefore, oxytocin was infused i.v. into conscious dogs in amounts calculated to give rise to plasma levels observed during physiological circumstances. Plasma levels of oxytocin, insulin, VIP (vasoactive intestinal polypeptide) and gastrin were measured by radioimmunoassay. When oxytocin was infused at a rate of 0.22 and 2.2 nmol kg-1 h-1, plasma oxytocin levels rose to 176 +/- 25 fmol ml-1 and to 1490 +/- 400 fmol ml-1, respectively, 10 min after the infusions were started. Plasma insulin levels rose in response to oxytocin administered at a rate of 0.22 and 2.2 nmol kg-1 h-1. A peak was recorded within 5 min of oxytocin infusion, that is, before maximal oxytocin levels were recorded, and basal levels were reached within about 20 min. The VIP levels rose slightly following infusion of oxytocin at 0.22 nmol kg-1 h-1, but a clear-cut response that lasted for 60 min was observed following infusion of oxytocin at the highest dose. In contrast, gastrin levels were not influenced by the oxytocin infusions. Suckling in dogs is followed by rapidly occurring short-lasting elevations of oxytocin levels in plasma which amount to 50-100 fmol ml-1. Since insulin and VIP were released by oxytocin when administered in amounts that give rise to plasma levels close to those levels, it is suggested that the secretion of insulin and VIP that occurs in response to suckling in lactating dogs may in part be caused by previously released oxytocin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Oxytocin infusions increase plasma levels of insulin and VIP but not of gastrin in conscious dogs. 390 74

The 24 endocrine pancreatic tumors and 14 carcinoids were examined immunohistochemically for cholecystokinin, insulin, gastrin, GIP, glucagon, sercretin, VIP, motilin, neurotensin, pancreatic polypeptide (PP), somatostatin, and ACTH. In 12 tumors of the pancreas more than one peptide-containing cell type was observed. The clinical symptoms showed hypersecretion of only one of the hormones, however. The midgut carcinoids (jejunum, appendix) represented the classical view of the carcinoid as an argentaffin cell tumor secreting 5-hydroxytryptamine. Tumors originating in the foregut (bronchus, stomach, duodenum) and hindgut carcinoids (rectum) were nonargentaffine, containing and secreting various polypeptide hormones. We conclude that light microscopic immunohistochemical methods are useful in distinguishing endocrine from nonendocrine tumors and multihormonal syndromes (MEA) in the classification of predominant hormone-secreting tumors.
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PMID:[Endocrine tumors of the gastrointestinal and pancreatic systems. Multiple endocrine adenoma from another viewpoint]. 610 39

Specific radioimmunoassay were used to measure somatostatin and vasoactive peptide in portal and peripheral plasma from conscious dogs prepared with indwelling portal catheters. In six animals with intact stomachs, a test meal induced a significant rise of portal and peripheral somatostatin, while the significant response of vasoactive intestinal peptide in portal plasma was not reflected in peripheral blood. Similar somatostatin and vasoactive intestinal peptide responses were observed in six dogs previously submitted to antrectomy and Billroth I anastomosis, when given the same test meal, while the gastrin response was 20% of the response in the intact dogs (P < 0.01). The effects of intragastric instillation of 300 ml dextrose, casein hydrolysate, and Intralipid, adjusted to 300 mosmol/kg and pH 7.0, were studied in six dogs with intact stomachs. Casein and Intralipid induced significant increases of somatostatin in portal and peripheral plasma, while VIP increased after Intralipid only, both in portal and peripheral blood. Dextrose resulted in no significant variation of either peptide in portal or in systemic plasma. Intraduodenal infusion of isotonic bile induced a significant release of somatostatin, both in portal and peripheral plasma, but no significant vasoactive intestinal peptide response. These results indicate that several factors can evoke a significant release of somatostatin in dogs, and that the variations of the peptide concentration in portal plasma are reflected in peripheral blood. Among the factors tested, only intragastric fat evoked a vasoactive intestinal peptide response that could be measured in peripheral blood.
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PMID:Effects of test meal, intragastric nutrients, and intraduodenal bile on plasma concentrations of immunoreactive somatostatin and vasoactive intestinal peptide in dogs. 610 20


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