Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Passive immunization with somatostatin (SRIF) antiserum suggests that gastrin, glucagon, and calcitonin secretion may be exerted either locally by contiguity of SRIF-like immunoreactivity (SRIF-LI)-containing D cells and G (gastrin) and A (glucagon) cells (paracrine) or by an endocrine effect. To determine whether a reciprocal relationship exists in man between these peptides and SRIF-LI, the effects of pentagastrin (0.5 microgram/kg BW), glucagon (1 mg), and calcium (15 mg/kg BW) on serum SRIF-LI were examined. The coexistence of SRIF-LI and calcitonin in normal thyroid parafollicular C cells and medullary carcinoma of the thyroid prompted a study of the effects of the known secretagogues of calcitonin, calcium (15 mg/kg BW), and pentagastrin (0.5 microgram/kg BW) on serum SRIF-LI. Sixteen normal subjects, two patients with metastatic medullary carcinoma of the thyroid, and one patient who had undergone thyroparathyroidectomy were evaluated. We demonstrated that whereas both pentagastrin and glucagon significantly elevated serum SRIF-LI, calcium infusion had no effect. Basal and stimulated SRIF-LI levels in the normal controls, patients with medullary carcinoma of the thyroid, and the patient with thyroparathyroidectomy were similar. These results suggest that SRIF-LI secretion is related to stimulation by peptides produced in closely juxtaposed cells, that SRIF-LI, unlike calcitonin, may not be a serum marker for medullary carcinoma of the thyroid in man, and that little, if any, serum SRIF-LI originates in the thyroid.
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PMID:Pentagastrin and glucagon stimulate serum somatostatin-like immunoreactivity in man. 610 30

The plasma levels of somatostatin (SRIF) were studied in normal subjects and patients with various disorders by a sensitive and specific radioimmunoassay. In 45 normal subjects, the fasting plasma SRIF concentrations were 13.3 +/- 5.3 pg/ml (mean +/- SD). Very high concentrations of plasma SRIF, ranging from 125.0 pg/ml to 400.0 pg/ml, were found in all four patients with medullary carcinoma of the thyroid examined and the SRIF levels were changed in parallel with their clinical course after resection of the tumor. A case of pheochromocytoma also showed a relatively high SRIF concentration in plasma (47.0 pg/ml), but the plasma SRIF level decreased to 8.7 pg/ml after removal of the tumor. In normal subjects, plasma SRIF levels did not fluctuate during 2 hr-observation period in basal state. Glucagon (1 mg, iv) and secretin (3 CHRU/kg B.W., iv infusion over 30 min) had no effect on the SRIF levels in the peripheral blood plasma of normal subjects. On intravenous infusion of arginine (0.5 g/kg B.W.) over 30 min, all 6 normal subjects showed a significant increase in plasma SRIF 30-45 min after the start of the infusion (basal value, 11.6 +/- 1.5 pg/ml; peak value, 27.2 +/- 3.0 pg/ml; p less than 0.005). Two cases of medullary thyroid carcinoma showed exaggerated responses after the arginine administration (increases of 103 pg/ml and 157 pg/ml, respectively), suggesting that SRIF was released from the tumor. The findings indicate that plasma SRIF determination in the basal state and after arginine administration is useful for detecting and following up SRIF-producing tumors.
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PMID:Plasma somatostatin in normal subjects and in various diseases: increased levels in somatostatin-producing tumors. 612 47

The secretagogue effect of histamine on calcitonin secretion has been studied in 15 patients with medullary thyroid carcinoma and compared with known stimuli: glucagon and calcium in combination with pentagastrin. The effect of concomitant histamine H2-receptor blockade on these responses has been studied in the same patients. Seven patients with undetectable basal plasma calcitonin concentrations had measurable responses to calcium/pentagastrin but not to histamine or glucagon. In the remaining eight subjects, significant responses were seen to all three test substances, calcium/pentagastrin proving to be the most potent secretagogue. Establishment of H2-receptor blockade with cimetidine had no effect on basal calcitonin concentrations and did not suppress responses to histamine, calcium or pentagastrin. The variable secretagogue effect of histamine could be mediated through H1-receptors, through nonspecific vascular dilation "washing out" preformed calcitonin, or through its destruction to varying degrees by histaminase, present in most medullary thyroid tumors. Histamine is unlikely to replace calcium/pentagastrin as the most discriminative, provocative diagnostic agent in medullary thyroid carcinoma, but correlation of secretory responses with tissue histaminase concentrations and attempted blockade with differing antihistamines will further our understanding of this tumor.
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PMID:Histamine and calcitonin release from medullary thyroid carcinoma. 613 Aug 34

Clinical and laboratory data, histologic, electron microscopic and immunocytochemical findings of the tumors of eight patients suffering from Cushing's syndrome and of one patient with hypercalcemia are described. The unlabeled antibody enzyme method was used for the detection of insulin, glucagon, somatostatin, pancreatic polypeptide, corticotropin, beta-lipotropin, calcitonin, parathyroid hormone, and gastrin. Ectopic Cushing's syndrome was caused by pancreatic endocrine tumors, medullary thyroid carcinoma, a bronchial, a gastric and a thymic carcinoid, and a carcinoid of the mediastinum. Hypercalcemia in one patient was related to a pancreatic endocrine tumor. After surgery the clinical symptoms disappeared in two patients, but persisted or relapsed in five patients. ACTH-immunoreactivity could be demonstrated in six of eight tumors; calcitonin-immunoreactivity was found in the tumor of the patient suffering from hypercalcemia. ACTH-immunoreactivity could be localized to secretory granules by immunoelectron microscopy, and the presence of ACTH and beta-LPH in the same tumor cells could be shown in one pancreatic tumor. A combination of production of orthotopic and ectopic hormones was found in one, and secretion of two ectopic hormones was detected in another pancreatic endocrine tumor.
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PMID:Ectopic hormone production by endocrine tumors: localization of hormones at the cellular level by immunocytochemistry. 627 90

In 12 patients treated 2 to 58 months previously for medullary carcinoma of the thyroid, basal serum concentrations of calcitonin, gastrin, vasoactive intestinal polypeptide, glucagon, insulin, and pancreatic polypeptide were measured in search of any correlation between these and the clinical course of the disease. All patients had elevated serum calcitonin levels indicating present disease. One patient had increased serum concentrations of several hormones. Another had achlorhydria and high serum gastrin levels. No relationship between calcitonin and gastro-intestinal polypeptides was found in 11 patients. No correlations were found between serum levels of polypeptides and the occurrence of diarrhoea in 5 patients. It is concluded that gastro-intestinal polypeptides, which are produced by other apudomas, are not secreted in more than normal concentrations under basal conditions, by the majority of patients previously treated for medullary carcinoma of the thyroid.
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PMID:Gastro-intestinal polypeptides in patients treated for medullary carcinoma of the thyroid. 637 28

The case of a 27 year-old woman with typical manifestations of multiple endocrine neoplasia type II b is reported. Medullary carcinoma of the thyroid was detected on the occasion of an operation for goiter when she was 22 years of age. Constipation due to megacolon caused by intestinal neuroma had persisted since childhood. Neuroma of the tongue and lips, hypertrophic corneal nerve and Marfanoid habitus were also found. The presence of pheochromocytoma was suggested in view of the positive cold pressor and results of glucagon loading tests, but this remains inconclusive. There was prolonged and exaggerated response of growth hormone and luteinizing hormone after provocative tests for anterior pituitary gland, in spite of normal basal levels. Screening of her family members for medullary carcinoma of the thyroid was carried out by measurement of immunoreactive calcitonin. Two siblings were shown to be hypercalcitoninemic, presumably due to occult medullary carcinoma of the thyroid. This case appeared to be the first in Japan showing multiple endocrine neoplasia type II b accompanied by familial hypercalcitoninemia.
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PMID:A case of multiple endocrine neoplasia type II b: endocrinological evaluation and family screening. 710 60

Pheochromocytoma accounts for about 0.1 per cent of patients with diastolic hyperstension. It mimics many diseases varying from anxiety psychoneurosis to intracranial tumors. Cardinal symptoms include sevre headache (72 to 92 per cent), sweating (60 tp 70 per cent), palpitations (51 to 73 per cent), and hypertension (> 90 per cent) of which 50 per cent is sustained, 50 per cent paroxysmal. Many drugs (phenothiazines, Saralasin, antiemetics, steroids, etc.) have been reported as precipitating factors. Patients who should be screened for pheochromocytoma include: (1) all symptomatic patients with sustained or paroxysmal hyperstension; (2) asymptomatic hypertension; (3) all patients with MEA 2a,b (hyperparathyroidism, medullary carcinoma of the thyroid, neurocutaneous lesions) and their first degree relatives, even if the latter are asymptomatic and normotensive; (4) hypertension plus diabetes mellitis or hypermetabolism; (5) hypertensive episode during induction of anesthesia or radiologic procedure; and (6) hypertensive response during histamine administration, i.e., gastric analysis. Urinary metanephrine is the single best screening test. Plasma catecholamine determination is particularly helpful when collected before and immediately after an attack. Provacative agents (histamine, glucagon, tyramine) are needed rarely. Preoperative localization of the tumor can be done with nephrotomography IVP, computerized axial tomography, ultrasound, 131-I-19-iodocholesterol scan, arteriography, venography.
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PMID:Pheochromocytoma: clinical manifestations and diagnostic tests. 745 90

Medullary thyroid carcinoma (MTC) can be important for gastroenterologists because 20-30% of patients with MTC suffer from chronic diarrhea and the tumor is capable of producing--besides other bioactive substances--a multitude of gastroenteropancreatic hormones. Gastrointestinal hormone profiles of 5 patients with MTC were determined both basally and after intravenous stimulation with secretin and calcium respectively. Diagnosis of MTC was confirmed histologically or cytologically and by demonstration of elevated serum concentration of calcitonin both basally and after calcium stimulation. 4/5 patients had chronic diarrhea. Normal values or only borderline increases were found for the following hormones: vasoactive intestinal polypeptide (VIP), neurotensin, substance P, growth hormone releasing hormone (GRH), glucagon, neurokinin A, peptide YY, and pancreatic polypeptide. Somatostatin was elevated after calcium stimulation in 1/5 patients only. The main findings were increased basal concentrations for GAWK in 5/5 patients and elevated concentrations for gastrin-releasing peptide (GRP, human bombesin) after calcium stimulation in 4/5. Probably as a consequence of the GRP increase, an increase in gastrin occurred in parallel, indicating bioactivity of the GRP released from the tumor. Besides calcitonin as the main tumor marker for MTC, determination of GAWK and GRP seems to provide helpful additional markers in laboratory diagnosis of MTC. GRP determination after i.v. calcium infusion allowed identification of patients with normal basal plasma GRP concentration.
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PMID:[Gastrointestinal hormone profile in medullary thyroid carcinoma]. 801 6

The effect of the adenosine A1 receptor activation on calcitonin secretion was studied in medullary thyroid carcinoma cells of the rat (rMTC 6-23). Calcitonin was determined by radioimmunoassay, intracellular cAMP by protein binding assay, intracellular calcium in fura-2 loaded single cells using microspectrofluorimetry, and calcium channel activity by patch clamp technique. The adenosine A1 receptor analogue N-6 phenylisopropyl-adenosine (PIA) (10(-10)-10(-6) M) inhibits dose-dependently glucagon (10(-7) M) and rGRH (10(-7) M) stimulated cAMP formation and calcitonin secretion. These effects were partly abolished by pretreatment with pertussis toxin (PT) (100 ng/ml). PIA (10(-10)-10(-6) M) also suppressed extracellular calcium-stimulated calcitonin secretion, rises in intracellular calcium, and calcium channel currents. PT (100 ng/ml) pretreatment again partly abolished this inhibitory effect. The addition to the medium of adenosine deaminase (0.4 U/ml) stimulated calcitonin secretion. Our results suggest that in calcitonin-secreting cells A1 receptors couple to adenylate cyclase and calcium channels via PT-sensitive G proteins and thus inhibit calcitonin secretion. Adenosine seems to act as an autocrine/paracrine factor in calcitonin-secreting cells.
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PMID:Adenosine A1-receptors inhibit cAMP and Ca2+ mediated calcitonin secretion in C-cells. 855 39

We have characterized, by RT-PCR amplification using specific primers, the presence of glucagon-like peptide-1 (GLP-I) receptor mRNA in CA-77 cells, a C cell line derived from a rat medullary thyroid carcinoma. Down-regulation of the GLP-1 receptor mRNA was observed after exposure of CA-77 C cells with GLP-1 (7-37). Increased secretion of both calcitonin gene-related peptide (CGRP) and calcitonin (CT) occurred after treatment with GLP-1 (7-37) associated with elevated steady-state levels of CGRP and CT mRNA. GLP-1 (7-37) increased cAMP formation in CA-77 cells in a dose-dependent manner; exendin (9-39), a GLP-1 receptor antagonist, inhibited cAMP production. The GLP-1 peptide which is produced by intestinal cells could be involved in the control of CT secretion through an entero-thyroidal axis implying GLP-1 receptor and increased CT gene expression.
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PMID:Expression of glucagon-like peptide 1 receptor in a murine C cell line: regulation of calcitonin gene by glucagon-like peptide 1. 881 99


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