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)

Angiographic findings in one giant cell carcinoma, one cystadenocarcinoma, one poorly vascularized mucinous cystadenocarcinoma, as well as in two avascular (gastrin- and glucagon-producing) islet-cell tumors of the pancreas are described. Two hypervascularized islet-cell tumors are presented for comparison and a case of tumorous chronic pancreatitis in a child is reported because ot its rarity. The aggressiveness of the giant cell carcinoma of the pancreas was demonstrated by its expansive growth. In the case of cystadenocarcinoma angiography revealed the tumor with hepatic metastases not diagnosed at explorative laparotomy. The relative hypovascularity in the case of mucinous cystadenocarcinoma was unusual. Both avascular islet-cell tumors simulated a pancreatic pseudocyst and the final diagnosis was made only by immunoassay. Chronic pancreatitis in a child presented with marked hypervascularization.
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PMID:Angiographic findings in some rare pancreatic tumors. 18 40

A reliable, sensitive, reproducible and specific radioimmunoassay for cholecystokinin-pancreozymin (CCK) has been developed, using rabbit antisera to highly purified porcine hormone. The natural occurring variant of CCK (39-CCK), in which the ordinary CCK is lengthened from its N-terminus by a hexapeptide, labelled with 125J, and repurified by column chromatography on Sephadex G-10 and on SP-Sephadex C-25, was used as tracer. Separation from antibody-bound labelled 39-CCK was carried out using a double antibody procedure. Non-specific interference with the assay system was abolished by ethanol extractions. Highly purified porcine CCK was used as standard. No significant crossreaction was found with gastrin, motilin, vasoactive polypeptide (VIP), gastric inhibitory polypeptide (GIP), natural and synthetic secretin, pancreatic glucagon or insulin. The sensitivity of the assay is approximately 40 pg/ml of test solution. The mean immunoreactive CCK concentration in 45 fasting normal subjects was 222 pg/ml increasing after food ingestion to 480 pg/ml. Somatostatin was able to abolish the stimulated CCK release. Elevated CCK concentrations were found in chronic pancreatitis. Immunohistochemical identification of pancreozymin cells was carried out either in surgical samples or in biopsy material. Approximately 1650 CCK cells per cross-section in the duodenum of humans have been found. The CCK cells usually appeared elongated, oval or pyramidal in shape and were observed to reach the lumen with their apical cell pole.
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PMID:Estimation of cholecystokinin-pancreozymin (CCK) in human plasma and tissue by a specific radioimmunoassay and the immunohistochemical identification of pancreozymin-producing cells in the duodenum of humans. 56 41

The response of serum immunoreactive gastric inhibitory polypeptide (IR-GIP), gastrin (IRG) and insulin (IRI) to a mixed standard meal was measured in 15 controls, 6 patients with coeliac disease, 26 patients with chronic pancreatitis and partial duodenopancreatectomy (Whipple's procedure). Serum levels of IR-GIP, IRG and IRI were significantly reduced in patients with coeliac disease. The serum glucose increase was significantly smaller only during the first hour after the meal. Since small intestinal GIP- and G-cells are situated mainly in the glands of duodenal and jejunal mucosa their absolute number is not significantly reduced in coeliac disease. It is suggested that the release of IR-GIP and duodenal IRG is influenced by the rate of absorption of nutrients. In patients with chronic pancreatitis the IR-GIP release is significantly greater than in controls, the IRG release normal and the IRI response delayed. After Whipple's procedure the IR-GIP response is increased significantly while the IRG secretion is abolished. This demonstrates that the duodenum is not necessary for GIP release and that pancreatic and jejunal gastrin are without clinical significance.
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PMID:Gastric inhibitory polypeptide (GIP), gastrin and insulin: response to test meal in coeliac disease and after duodeno-pancreatectomy. 95 38

On the basis of some experimental observations of hypergastrinemia in animals chronically intoxicated with ethanol, both fasting and after meals serum gastrin were determined in patients affected by chronic alcoholic pancreatitis. A significant increase in serum gastrin levels was observed in patients with chronic pancreatitis compared with controls, both in basal conditions and following food stimulation. The physiopathological hypotheses and possible aetiopathogenetic implications suggested by such gastrin behaviour are discussed.
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PMID:[Chronic alcoholic pancreatitis and blood gastrin]. 96 55

Twenty-nine patients with chronic pancreatitis had a significantly greater IR-GIP response to a test meal than 15 controls. This increased response was not related to the degree of steatorrhoea or glucose intolerance. It was most marked in a group of patients with moderately impaired IRI release and medium steatorrhoea. From this is concluded that the IR-GIP response to a test meal is determined by at least two factors: 1. feedback control via insulin secretion, 2. assimilation of fat. In chronic pancreatitis endocrine insufficiency may induce an exaggerated GIP response and severe exocrine insufficiency may prevent fat induced GIP release. Gastrin is not involved in the different GIP response in patients with chronic pancreatitis.
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PMID:Response of gastric inhibitory polypeptide (GIP) to test meal in chronic pancreatitis--relationship to endocrine and exocrine insufficiency. 100 49

Morphology of pancreas (either esocrine, either endocrine) was studied in 29 cases of surgically treated chronic pancreatitis (27 cases of chronic calcifying pancreatitis and 2 cases of chronic obstructive pancreatitis). Parenchymal sclerosis in chronic calcifying pancreatitis (CCP) which represents the goal of our study was graded as mild (10 cases), moderate (10) and severe (7). Immunoperoxidase staining (PAP method) for insulin, glucagon, somatostatin, pancreatic polipeptide (PP), vasoactive intestinal polipeptide (VIP) and gastrin, was used to investigate endocrine pancreas. Acinar sclerosis and endocrine damage were closely related. Progression of sclerosis into islet appears to follow vascular pedicles producing a fragmentation into small cell groups as final result. In all cases of moderate or severe sclerosis, A/B cell ratio was increased due to the reduction of insulin positive cells. "Adenoma-like complexes", i.e., apparent concentration of islets, resulting from the loss of the acinar component, were observed in 7 cases with moderate or severe sclerosis. Nesidioblastosis was a prominent feature in all cases but one, with a positivity for insulin in 11 cases, for glucagon in 13, for somatostatin in 6 and for PP in 17. No positivity for gastrin was observed, while VIP was detected in a few ganglia. An increased amount of PP cells in islet and budding from the ducts was noticed and their presence outside the pancreatic head was demonstrable in 4 out of the 7 distal pancreatectomy specimens. Our data confirm the secondary involvement of the endocrine pancreas in the sclerotic acinar process.
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PMID:[Anatomopathologic pictures of chronic pancreatitis]. 209 39

A disturbed intraduodenal milieu and pancreatic scarring in advanced chronic pancreatitis (CP) may lead to changes of gut and pancreatic hormones. In the present study, the gastroduodenal mucosal content of several regulatory peptides was determined in 8 patients with severe calcific CP and 8 healthy volunteers. In addition, hormone release into the bloodstream was estimated after intraduodenal acid/glucose stimulation in the control subjects and 8 CP patients each with or without secondary diabetes mellitus (DM), and in 8 patients with juvenile DM, so that disturbed gut hormone release could be attributed either to CP or DM. While VIP release into the circulation was similar in all participants, mucosal levels of VIP and substance P were significantly elevated in the duodenal bulb and descending duodenum of CP patients. The somatostatin content of gastroduodenal mucosa in CP was at least as high as in normals. Gastrin was significantly more abundant only in the duodenal bulb of CP patients, while plasma gastrin was normal. Duodenal CCK concentrations tended to be elevated in the duodenal bulb, but not significantly. The release of secretin seemed to be higher in type-1 diabetics than in CP patients. The mucosal pattern of GIP was nearly identical in CP patients and controls. Compatible with this finding, the GIP release did not show any peculiarities in CP with or without DM or in DM. Basal and stimulated plasma levels of motilin were abnormally high in CP. Pancreatic polypeptide plasma levels were normal in DM, but significantly reduced in CP, especially in CP with DM. Fasting PP and stimulated pancreatic enzyme outputs were linearly related.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chronic pancreatitis and diabetes mellitus: plasma and gastroduodenal mucosal profiles of regulatory peptides (gastrin, motilin, secretin, cholecystokinin, gastric inhibitory polypeptide, somatostatin, VIP, substance P, pancreatic polypeptide, glucagon, enteroglucagon, neurotensin). 246 85

The present study was designed to examine and compare the peptide composition and relative immunochemical purity of GIH and Boots secretin preparations. Gastrointestinal peptides were measured by radioimmunoassay using antibodies to secretin, gastrin, immunoreactive cholecystokinin, vasoactive intestinal peptide, gastric inhibitory peptide, and somatostatin. Boots secretin was found to contain substantial quantities of gastrin, immunoreactive cholecystokinin, vasoactive intestinal peptide, gastric inhibitory peptide, and somatostatin. In contrast, GIH secretin contained only a very small amount of vasoactive intestinal peptide. GIH also contained approximately three to four times more secretin per unit as did Boots secretin. Intravenous infusion of Boots, but not GIH, secretin in seven healthy volunteers produced significant increases in venous plasma of all peptides. Results of these studies indicate that Boots secretin contains large and variable quantities of gastrointestinal peptides other than secretin and that the contents of both secretin and the other peptides vary among different lots. Because the quantity of these peptides is sufficient to increase significantly their blood levels and consequent biological effects, it is concluded that GIH is preferable to Boots secretin in the clinical evaluation of patients with suspected chronic pancreatitis or gastrinoma.
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PMID:Peptide characterization of secretin preparations. 286 51

A patient with a calcifying chronic pancreatitis was found to have a neuroendocrine islet cell tumour (a previously unreported association). The tumour secreted both gastrin and ACTH leading to clinical manifestations of both the Zollinger-Ellison syndrome and Cushing's syndrome.
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PMID:Neuroendocrine islet cell tumour producing gastrin and ACTH in a patient with calcifying chronic pancreatitis. 298 96

The effect of combined use of pentoxifylline and solcoseryl was studied in 35 patients with chronic pancreatitis. General clinical findings were studied in parallel with the time course of pancreatic exocrine (trypsin) and endocrine (insulin, C-peptide) function. The blood level of gastrin and changes in intestinal function using 131I-lipids were also studied. The incorporation of both drugs in multimodality therapy made a positive therapeutic effect, resulting in a decrease in the pain syndrome and dyspeptic symptoms. At the same time some favorable shifts in pancreatic and GI tract function were noted. Possible mechanisms of a positive therapeutic effect were discussed. A conclusion was made that the incorporation of pentoxifylline and solcoseryl in multimodality therapy of chronic pancreatitis was clinically justified and determined pathogenetically.
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PMID:[Trial of the combined use of trental and solcoseryl in treating patients with chronic pancreatitis]. 336 55


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