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 effects of 48 days of streptozotocin-induced diabetes mellitus in rats on plasma concentrations of gastrin, somatostatin, pancreatic glucagon, and enteroglucagon have been assessed. In addition, neuroendocrine changes in sections of gastric mucosa were quantified using a computer-assisted morphometric system following immunohistochemical staining with polyclonal antibodies directed against gastrin, PGP 9.5 (a neural protein), and somatostatin. Diabetes resulted in significantly increased fasting plasma concentrations of somatostatin, and entero- and pancreatic glucagon. In contrast, lower plasma gastrin concentrations and decreased antral G-cell density were noted in diabetic rats. Gastric somatostatin and neuronal PGP 9.5 stain densities were unaltered by diabetes. Stomachs of diabetic rats weighed less, but both the jejunum and ileum showed evidence of mucosal hyperplasia. The gastric neuroendocrine atrophy observed in diabetes may be a consequence of elevated plasma somatostatin derived from nongastric sources. The enhanced growth of the intestinal mucosa may be related, directly or indirectly, to raised intraluminal glucose concentration in diabetes.
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PMID:Neuroendocrine changes in rat stomach during experimental diabetes mellitus. 156 19

Three cases of carcinoid tumour of the stomach associated with primary hyperparathyroidism had the clinical and pathological features of a pluriglandular syndrome. Two of the patients showed multiple small polypoid carcinoids in the non-antral stomach, in conjunction with a parathyroid adenoma in one and parathyroid hyperplasia in the other case. One of these patients was also suffering from pernicious anaemia. A third patient had a large metastasising carcinoid arising in the gastric body and a parathyroid adenoma. Immunohistochemical stains for PGP 9.5 were positive in the carcinoids of all three cases. In all cases the carcinoids showed immunoreactivity for gastrin. A positive family history of endocrine hyperplasia and neoplasia was established in one case. It is suggested that patients with gastrointestinal carcinoids and their families should be evaluated for hyperparathyroidism, and patients with hyperparathyroidism presenting with upper gastrointestinal symptoms should undergo endoscopy to rule out gastric carcinoid tumours.
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PMID:Carcinoid tumour of stomach and primary hyperparathyroidism: a new association. 295 64

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

The presence of distribution of several neurochemical markers in human fungiform papillae and taste buds were investigated by the immunohistochemical technique. The gustatory cells of the taste buds are in synaptic contact with sensory nerve endings, and considering the taste buds strictly as specialized sensory organs, the amounts and distribution of some of the neurochemical markers were different to what we expected. For example, few structures showed immunoreactivity to the tachykinins substance P (SP), calcitonin gene-related peptide (CGRP), and neurokinin A (NKA) also for the peptides vasoactive intestinal polypeptide (VIP), neuropeptide tyrosine (NPY) and galanin, low amounts of immunoreactivity occurred. On the other hand, using antibodies to protein gene product 9.5 (PGP 9.5), protein S-100, and glutamate, numerous nerve fibres and/or immunoreactive cells were found in the fungiform papillae, in the epithelium, in the connective tissue and around blood vessels, as well as in or near taste buds. Incubation with the antibodies against somatostatin, enkephalin, bombesin, peptide histidine isoleucine amide (PHI), cholecystokinin (CCK)/gastrin and dopamine-beta-hydroxylase (DBH) was negative for the fungiform papillae. In conclusion, the present study has shown several immunoreactive structures using antibodies against certain neurochemical markers. Further investigations will hopefully correlate these morphological findings with functional taste perception data. Future studies of patients with taste disorders or other pathological changes correlated with taste and tongue will also be of utmost importance.
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PMID:Neurochemical markers of human fungiform papillae and taste buds. 857 44

The occurrence and distribution of several neurochemical markers were investigated. Numerous nerve fibres were shown, using antibodies to protein gene product (PGP) 9.5, neurone-specific enolase, calcitonin gene-related peptide (CGRP), substance P. neurokinin A or protein S-100. The presence of vasoactive intestinal polypeptide (VIP), peptide histidine isoleucine amide (PHI), neuropeptide tyrosine, dopamine-beta-hydroxylase (DBH), cholecystokinin/gastrin, glutamate and galanin was more scarce. Nerve fibres containing these above-mentioned markers were found at several locations, i.e. in the epithelium, connective tissue, and around blood vessels. In the taste buds, numerous PGP 9.5, neurone-specific enolase-, CGRP-, substance P-, neurokinin A- and protein S-100-containing structures were found, but few VIP and galanin ones. No immunoreactivity was found with antibodies against somatostatin, bombesin, enkephalin or dynorphin. These findings extend knowledge about the general as well as the neurochemical messenger-based innervation of rat fungiform papillae, forming a firm basis for future functional investigations of normal, experimental and also clinical materials.
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PMID:An immunohistochemical screening of neurochemical markers in fungiform papillae and taste buds of the anterior rat tongue. 913 26

RT-PCR-based amplification of transcripts expressed in cancer but not in normal non-neoplastic cells is increasingly used for the sensitive detection of rare disseminated or exfoliated cancer cells to improve cancer staging and early detection protocols. However, these assays are frequently hampered by false-positive test results due to low-level transcription of the marker genes in normal cells. To overcome these limitations, target transcripts have to be identified that are tightly suppressed in normal non-neoplastic tissues, whereas they should be actively transcribed in the respective cancer cells. Here, we tested RT-PCR assays for 7 neuroendocrine marker transcripts including NCAM, PGP 9.5, gastrin, gastrin receptor, synaptophysin, preprogastrin-releasing peptide (preproGRP) and GRP-receptor to detect rare exfoliated tumor cells in peripheral venous blood and sputum samples from patients with lung cancer. Among these preproGRP RT-PCR was the only assay with which illegitimate transcription in blood or sputum samples from healthy donors or patients with unrelated diseases did not interfere. However, it reproducibly detected up to 10 small-cell lung cancer cells diluted in either 10 ml blood or 5 ml sputum samples. Single blood and sputum samples were collected directly before diagnostic bronchoscopy from 175 patients suspected to have lung cancer. Twenty-six of these had small-cell lung cancer (SCLC). Thereof, 13 patients (50%) tested positive in the blood sample and 5 of 23 patients (22%) tested positive in the sputum sample. Moreover, among 92 patients with non-small-cell lung cancer (NSCLC) 25 patients (27%) had disseminated cancer cells in peripheral blood. Amplification of preproGRP transcripts from clinical samples is a sensitive and specific assay to detect disseminated or exfoliated lung cancer cells either in peripheral blood or sputum samples.
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PMID:Sensitive detection of rare cancer cells in sputum and peripheral blood samples of patients with lung cancer by preproGRP-specific RT-PCR. 1127 99

The mechanism of islet neogenesis remains poorly understood, despite its potential applications in regenerative or replacement therapies for the treatment of insulin-dependent diabetes. During fetal development of the mouse or rat, the majority of islet cells are formed in late gestation (E18-21) by the process of neogenesis from precursor cells. The precursor cells are organized as ducts that actively proliferate and express high levels of specific cytokeratin (CK) proteins. Transitional cells coexpressing islet hormones and CK are frequent and disappear shortly after birth, to reappear only in conditions in which pancreas or islet regeneration has been induced. Islet morphogenesis is thought to operate mainly through the budding of islet cells from ducts, followed by their migration away from the duct to form clusters. Single islet cells are indeed frequent in the fetal and regenerating pancreas, but they also occur in normal tissue, especially in the human pancreas. A different neogenic mechanism, observed in the fetal rat, consists in the proliferation of ductal cells resulting in large aggregates. Starting from the middle of the aggregate, cells differentiate into islet cells and gradually lose their proliferative activity and other ductal characteristics. In adult pancreas, islets are in close contact with at least one duct or ductule. Such a direct duct-islet axis becomes even more evident in regeneration models, such as duct ligation. In these models, a metaplastic transformation of the exocrine pancreas to so-called pseudoductal complexes is seen. Surviving exocrine cells acquire a metaplastic phenotype, which resembles the fetal protodifferentiated state. They start to express CK, the beta-cell transcription factor Pdx1, the neuroendocrine/islet cell markers PGP9.5 and the CCKB receptor for gastrin, and they show pronounced proliferative activity and islet neogenesis. We hypothesize that these de-differentiated or metaplastic exocrine cells (acinar and ductal), acquire a multipotential state and can serve as islet precursors.
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PMID:Islet morphogenesis and stem cell markers. 1528 45

Researches on spicatoside A (SpiA)-containing natural products suggest the possibility of SpiA as a potential laxative to alleviate chronic constipation. However, no studies have been conducted with single compound administration of SpiA. To verify the laxative effects and mechanism of action of SpiA on chronic constipation, we investigated alterations in the excretion parameters, histological structure, and cholinergic regulation of the enteric nerve in the colons of Institute of Cancer Research (ICR) mice with loperamide (Lop)-induced constipation after exposure to 20 mg/kg of SpiA. Decrease in the number, weight and water contents of stools in the Lop+Vehicle treated group significantly recovered after SpiA treatment, and alterations in the histological structure and transmission electron microscopy (TEM) images were improved in the Lop+SpiA treated group. Similar recovery effects were observed in the ability for mucin secretion and expression of the membrane water channel gene (aquaporin 8, AQP8). Furthermore, significant improvements were observed in the acetylcholinesterase (AChE) activity and acetylcholine receptors' (AChRs) downstream signaling pathway after treatment of SpiA. The levels of gastrointestinal (GI) hormones including cholecystokinin (CCK) and gastrin were also remarkably enhanced in the Lop+SpiA treated group as compared to the Lop+Vehicle treated group. The expression of receptor tyrosine kinase (C-kit) and protein gene product 9.5 (PGP9.5) in Cajal and neural cells, as well as the phosphorylation of myosin light chain (MLC) in smooth muscle cells, were recovered after SpiA exposure. Taken together, the results of the present study provide the first strong evidence that SpiA improves chronic constipation through muscarinic cholinergic regulation of the enteric nerve in a Lop-induced constipation ICR mice model.
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PMID:Laxative Effect of Spicatoside A by Cholinergic Regulation of Enteric Nerve in Loperamide-Induced Constipation: ICR Mice Model. 3083 59