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)

Functioning tumors of the pancreatic islets are now recognized as the source of clinical syndromes affecting the gastrointestinal tract which have a wide variety of catastrophic symptoms. Experiences with thirty-six cases suggest at least four separate diagnostic categories in the ulcerogenic tumor syndrome. These include: a typical history, gastric analysis, and roentgenographic findings with boderline fasting serum gastrin levels; ulcerogenic tumor with evidence of hyperparathyroidism; iatrogenic ulcerogenic syndrome associated with failure of a previous operation for duodenal ulcer; and the classic ulcerogenic syndrome associated with a fulminating ulcer diathesis or diarrhea and high serum gastrin levels. The problems presented at operation include: decisions to be make in the presence of a negative exploration; the finding of a solitary tumor in the wall of the duodenum; solitary pancreatic tumors particularly in the body and tail; ulcerogenic tumors in the very young; liver metastases in the elderly; and the wisdom of removing gross metastases in combination with total gastrectomy. The long-term survival in the ulcerogenic tumor syndrome approximated 50 per cent, with 40 per cent of those having proved malignancy living five years. Evidence of hyperparathyroidism is relatively common in association with both the ulcerogenic and the diarrheogenic tumor syndromes. The association may by a result of a congenital abnormality, metabolic alkalosis, or a direct effect of the islet cell tumor. Parathyroidectomy may be indicated when both the serum calcium and parathormone levels are elevated in the presence of borderline fasting gastrin levels. The latter may return to normal after parathyroidectomy. The evidence of hyperparathyroidism closely parallels the episodes of diarrhea in the diarrheogenic syndrome, and hyperparathyroidism may regress spontaneously after total removal of the pancreatic tumor. Just as routine calcium determinations made the diagnosis of hyperparathyroidism more commonplace, it is suggested that the gastrointestinal syndromes associated with islet cell tumor would receive wider recognition if radioimmunoassays for gastrin as well as secretin, and the other secretin-like polypeptides, were carried out routinely.
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PMID:Islet cell tumors of the pancreas and the alimentary tract. 16 36

The parathyrin receptor in renal cortex has been investigated by studying the binding of 125I-labelled parathyrin, or of unlabelled parathyrin detected with 125I-labelled antibodies, to a partially purified plasma membrane fraction. The kinetics of hormone uptake demonstrated a biphasic response in both systems at 22 degrees C but this phenomenon was not detectable at 37 degrees C. Specific displacement of lactoperoxidase labelled 125I-labelled parathyrin occurred with 8 ng unlabelled bovine parathyrin. The apparent affinity constant was 2.3-10(8) M(-1) and the apparent binding capacity of the membranes 1.25 pmol/mg protein. Using the labelled antibody technique the receptor showed maximal binding at pH 7.0-7.5. As little as 80 pg bovine parathyrin produced a significant increase in binding of labelled anti-bovine parathyrin antibody and saturation of binding sites was demonstrated at 2.5 pmol/mg protein. Oxidized hormone showed undetectable binding. Treatment of membranes with phospholipases A or D, or Trypsin greatly reduced subsequent hormone binding. Prior incubation of membranes with 1-34 synthetic parathyrin decreased the binding of intact hormone whereas gastrin, insulin and glucagon had no effect. Growth hormone and calcitonin slightly increased parathyrin binding.
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PMID:Characterization of the parathyrin receptor in renal plasma membranes by labelled hormone and labelled antibody binding techniques. 17 66

Stimulation of the beta-adrenergic terminations was employed to determine whether calcitonin-secreting thyroid C cells are derived from the neural crest. Calcitonin secretion was increased, whereas parathormone, insulin and gastrin values were not significantly changed. In addition, administration of a beta-blocking drug before ethanol led to a marked fall in calcitonin with respect to the baseline. Once again, other hormone levels were not affected.
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PMID:[Calcitonin, gastrin, parathyroid hormone and the autonomic nervous system]. 20 23

The relations of calcitonin concentrations to the presence of bone marrow metastases and to the concentrations of calcium, parathormone and gastrin in serum were investigated in 74 untreated patients with small cell carcinoma of the lung. Calcitonin concentrations were enhanced in two thirds of the patients, while serum calcium concentrations were normal in all. In 19 of 57 patients parathormone concentrations were slightly above the normal range, but the concentrations of parathormone and calcitonin were not correlated. Bone marrow metastases had no influence on the concentration of serum calcitonin. Finally, a small inverse correlation between the concentrations of gastrin and calcitonin in serum was observed. The results resemble those of the calcitonin-producing medullary carcinoma of the thyroid, supporting the suggestion of an ectopic source of hypercalcitoninemia in small cell carcinoma of the lung.
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PMID:Small cell carcinoma of the lung: relation of calcitonin to bone marrow metastases, parathormone and gastrin. 22 33

Foregut endocrine polypeptide-secreting APUD cells (Amine-Precursor-Uptake and Decarboxylation), in their embryologic migration from neural crest to foregut may become "arrested" in the mesoderm or in other ectopic locations. They may become hyperplastic, adenomatous or malignant. Eight illustrative patients are reported. One patient had "pancreatic hyperparathyroidism" with hypercalcemic crises, pancreatic apudocarcinoma, normal parathyroids, biologically active parathormone, but inert immunochemically to the usual parathyroid antisera. Two had gastrin-secreting malignancies in the mesoderm. Remission after excision, but eventual recurrence of the syndrome due to islet cell hyperplasia required total gastrectomy. One patient had a gastric corpus apudocarcinoma found prospectively with hypergastrinemia which required excision of the tumor. One patient had acromegaly with hypergastrinemia and antral gastrinosis treated by pituitary irradiation, One patient had the antral or intermediary type of the Zollinger-Ellison syndrome with moderate hypergastrinemia, duodenal ulcer and antral gastrinosis, treated by vagotomy and antrectomy. One patient had hyperparathyroidism with antral gastrinosis, treated by parathyroidectomy. One patient had malignant Zollinger-Ellison syndrome and developed associated thyroid parafollicular cell hyperplasia and parathyroid chief cell hyperplasia, treated by total gastrectomy and multiple endocrine excisions. These investigative observations demonstrate ectopic loci and associated hyperplasias which support the concept of migration and bizarre potentiality of polypeptide-secreting cells of the foregut.
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PMID:Ectopic apudocarcinomas and associated endocrine hyperplasias of the foregut. 24 2

Antral somatostatin- and gastrin-producing cells (D and G cells) were studied in a group of patients with chronic renal failure (CRF) in comparison with a control group. Gastric acid secretion and serum gastrin, phosphate, and parathormone (PTH) levels were also evaluated in every patient. The group with CRF showed a mild increase both in G- and in D-cell denisty. In this group serum phosphate and PTH levels were higher than normal, showing hyperparathyroidism in every patient. A direct correlation was found between G-cell density and parathyroid function in patients with CRF. Hyperparathyroidism, therefore, seems to play a role in the mechanism of increased serum gastrin levels in CRF.
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PMID:Antral G- and D-cell counts in chronic renal failure. 37 75

A patient with the Zollinger-Ellison syndrome was found to have increased blood gastrin levels associated with the secretion of a compound which produced high blood calcium levels. This compound differed from immunoreactive parathormone, and caused the clinical picture of primary neoplastic hyperparathyroidism. This case is compared with other cases of multiple-secreting Zollinger-Ellison syndrome reported in the published literature, within the framework of the "A.P.U.D." system.
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PMID:[Zollinger-Ellison syndrome with high blood calcium levels resembling the neoplastic type (author's transl)]. 47 10

To define the relationship between hyperparathyroidism (HPT) and gastric function, 31 patients with HPT were prospectively studied before and 2 to 25 months after parathyroidectomy. The gastrin response to a standard test meal (STM), the basal acid output (BAO), and the peak acid output (PAO) were determined. Parathormone and calcium were elevated in all patients and returned to normal following parathyroidectomy. The mean fasting gastrin concentration, mean integrated gastrin response (IGR) to feeding, mean basal acid output (BAO), and mean peak acid output (PAO) were not changed by successful parathyroidectomy. There was no significant correlation between gastrin concentration or gastrin response to feeding and gastric acid secretion. Eight of 31 HPT patients had fasting gastrin concentrations above normal preoperatively and remained so postoperatively. Hypergastrinemia in six of these eight patients could be explained by the Zollinger-Ellison (Z-E) syndrome or chronic atrophic gastritis. The hypothesis that peptic ulcer disease seen in some HPT patients is the result of calcium-induced hypergastrinemia causing gastric hypersecretion is not supported by this study.
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PMID:Does hyperparathyroidism cause hypergastrinemia? 94 Oct 95

Gastric secretion was evaluated in 9 male patients with chronic renal failure on maintenance hemodialysis. Five secreted low or normal quantities of acid and 4 exhibited hypersecretion, 2 of whom had associated peptic ulcer disease. Serum gastrin responses to a protein meal were comparable to control subjects. Calcium infusion in two basal hypersecretors depressed acid secretion. The only statistically significant correlation observed was between basal acid output ans serum levels of parathormone. These studies suggest that while acid secretory abnormalities vary in patients with chronic renal failure on hemodialysis, there is no apparent sensitivity of the gastrin-secreting cells to protein or calcium ion which might account for acid hypersecretion. Secondary hyperparathyroidism may influence the occurrence of acid secretory abnormalities.
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PMID:Gastric secretory function in patients with chronic renal failure undergoing maintenance hemodialysis. 101 5

According to previous investigations, ricin the toxic protein of castor oil seeds (Ricinus communis, Euphorbiaceae) given in subtoxic dose, evokes a parathyroid lesion with a consecutive parathormone mobilization in the rat. The elevated parathormone level rises the plasma calcium-content resulting (among others) in endogenous gastrin mobilization. This latter increases the gastric acid secretion in significant degree. This, hitherto unknown effect of ricin directs the attention once again to the complexity of its toxic action.
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PMID:In experimental ricin intoxication there is a detectable gastric acid secretion in the rat. 130 82


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