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)

We treated four patients who had hypoglycemia and nonpancreatic tumors. Two had pleural mesothelioma, one had primary fibrosarcoma of the liver, and one had pheochromocytoma metastatic to the liver. We propose four mechanisms for this syndrome: (1) insulin or insulin-like activity produced by the tumor, (2) decreased gluconeogenesis, (3) disruption of glucagon metabolism, and (4) increased utilization of glucose by the tumor. The local effects of the tumor in hepatic parenchyma may also play an important role. The important diagnostic tests are an insulin-glucose ratio, to rule out insulinoma, and fasting glucose levels. An assay of nonsuppressible insulin-like activity can be performed and is of investigative interest, but does not aid in individual patient therapy. Treatment consists of control of the tumor.
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PMID:Causes and evaluation of tumor-induced hypoglycemia. 709 41

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 scanning using 131J-meta-benzylguanidine was done in one patient with metastasizing paraganglioma, one patient with multiple endocrine neoplasia type IIb. No activity of tumour tissue could be demonstrated in the patient with metastasizing paraganglioma, whereas the pheochromocytoma could be clearly defined in the patient with multiple endocrine neoplasia type IIa. The female with multiple endocrine neoplasia type IIb showed a suspect space-occupying lesion of the left adrenal using computed tomography. Pheochromocytoma could be excluded by 131J-benzylguanidine scanning, selective estimation of catecholamines in adrenal venous blood as well as the glucagon stimulation and clonidine suppression.
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PMID:[Imaging adrenergic tumours with 131J-meta-benzylguanidine]. 711 46

In more than half of 67 patients suspected of having pheochromocytoma, glucagon stimulation increased plasma free norepinephrine (NE) and epinephrine (E) 50% or more, with rising blood pressure or pulse rate; only three patients, however, harbored a pheochromocytoma. A low degree of catecholamine conjugation accounts for most of the false-positive results. In patients with low conjugated NE +E there was a greater rise in free NE +E and free E as well as in pulse rate after glucagon stimulation than in those with normal levels of conjugated NE+E. Glucagon-sensitive adenylate cyclase was found in pheochromocytomas but not in a functional adrenocortical adenomas. After sham administration of glucagon, there were rises in blood pressure but not in free NE or E in four patients. The glucagon-induced catecholamine test can be false-positive in hyperadrenergic essential hypertensive patients with abnormally low conjugated NE +E. Saline alone in a sham glucagon test in susceptible patients raises systolic blood pressure and pulse rate, and therefore, if plasma free NE and E are measured and found not to rise this type of false-positive result can be eliminated.
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PMID:Basis of false-positive glucagon tests for pheochromocytoma. 721 98

The effects of glucagon on the adrenergic system have been studied in experimental and clinical conditions. 1. in vitro studies: In the first experiment a continuous flow incubation system was developed in which the secretory response to these drugs was characterized by a serial fluorimetric assay of catecholamines in the effluent medium. Pig adrenal medulla or human pheochromocytoma were studied. There was an initial massive release of catecholamines which declined to basal levels (0.02 micrograms/mg) after 1.5 hours. When 10(-4) glucagon was infused for 10 minutes following 2 hours of preincubation, both adrenaline and nonadrenaline outputs rose abruptly to concentrations of 0.08 micrograms/mg and 0.07 micrograms/mg respectively. In the second experiment the effect of these drugs on the in vitro release of catecholamines from the isolated in vitro chromaffin granules of the pig adrenal medulla were studied. The results were the same as in the previous experiment. 2. clinical studies: The effects of glucagon were studied on the blood pressure and urinary catecholamine levels of healthy control subjects, of patients suffering from essential hypertension, thyroid disease, diabetes mellitus and acromegaly. Glucagon induced a slight but constant increase in blood pressure. By contrast no significant urinary catecholaline elevation was evoked. There was no difference in the effect of intravenous glucagon between normal subjects and patients suffering from the above-mentioned disorders.
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PMID:[A reevaluation of the glucagon provocative test for pheochromocytoma--on the in vitro release of catecholamine from the adrenal medulla or pheochromocytoma tissue, and on the effect of intravenous glucagon on urinary catecholamine excretion and blood pressure (author's transl)]. 740 74

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

Pheochromocytoma is mainly characterized by a great deal of variability in its biological activity and in its clinical manifestations. This special feature has always to be taken into account in any diagnostic procedure. The tumor is generally suspected on clinical ground for the presence of paroxysmal hypertension but this sign is largely aspecific and often absent. The diagnosis of pheochromocytoma has to be based on laboratory tests demonstrating an excess and/or a disregulation in catecholamine (CA) secretion. CA or CA metabolites can be measured in urine or blood. Whatever the sample measured, it is important to correlate its result with the clinical picture found during its collection. Basal plasma CA concentrations are often raised also during periods of normotension but their accuracy is the highest in samples drawn during a hypertensive crisis. When basal measurements are insufficient for a final diagnosis, inhibitory (clonidine) or stimulatory (glucagon) tests can be performed. Clonidine test is recommended in patients showing slight increases in basal plasma CA. Glucagon stimulation test should be performed only in normotensive patients with an incidental adrenal mass, patients with sporadic hypertensive crises or members of families affected by MEN II. Localization procedures are mainly based on CT (or MRI) and on scintigraphy with I131-MIBG. CT possesses high sensitivity (about 96%) while I131-MIBG scintigraphy possesses a very high specificity (about 97%). Therefore, both the procedures should be performed before surgery. Rarely, it is also necessary to perform catheterization of the venous tree and plasma sampling for CA measurement to localize the tumor through the discovery of a secretory gradient.
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PMID:[Diagnostic problems in pheochromocytoma]. 765 Dec 83

A number of endocrine disorders are associated with varying degrees of glucose intolerance. Sustained hypersecretion of hormones with actions antagonistic to insulin (e.g., GH, glucocorticoidos, catecholamines, glucagon) or which interfere with insulin secretion (e.g., catecholamines, hypokalemia) is often associated. And so, acromegaly, Cushing's syndrome, pheochromocytoma, primary aldosteronism, hyperthyroidism, glucagonoma and others are included in endocrine-associated diabetes. The glucose intolerance occurring secondary to endocrine disorders is usually moderate degree and overt diabetes with symptomatic hyperglycemia is an uncommon event, unless an underlying genetic diabetic diathesis also present in the same individual. The small subgroup of acromegalics(5-10%) with severe glucose intolerance requiring insulin therapy have low endogenous insulin levels and insulin responses that are markedly impaired. It has been suggested that these patients are really true diabetics. These are patients with NIDDM. Retinal, renal and neurological complications are uncommon in patients with endocrine-associated diabetes.
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PMID:[Diabetes secondary to endocrinolopathies]. 891 32

Pancreatic beta cells (insulin-producing cells) and neuronal cells share a large number of similarities. Here, we investigate whether the same mechanisms could control the expression of neuronal genes in both neurons and insulin-producing cells. For that purpose, we tested the role of the transcriptional repressor neuron-restrictive silencing factor/repressor element silencing transciption factor (NRSF/REST) in the expression of a battery of neuronal genes in insulin-producing cells. NRSF/REST is a negative regulator of the neuronal fate. It is known to silence neuronal-specific genes in non-neuronal cells. We demonstrate that, as in the case of the neuronal pheochromocytoma cell line PC12, mRNA coding for NRSF/REST is absent from the insulinoma cell line INS-1 and from three other insulin- and glucagon-producing cell lines. NRSF/REST activity is also absent from insulin-producing cell lines. Transient expression of REST in insulin-producing cell lines is sufficient to silence a reporter gene containing a NRSF/REST binding site, demonstrating the role of NRSF/REST in the expression of neuronal markers in insulin-producing cells. Finally, by searching for the expression of NRSF/REST-regulated genes in insulin-producing cells, we increased the list of the genes expressed in both neurons and insulin-producing cells.
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PMID:Expression of neuronal traits in pancreatic beta cells. Implication of neuron-restrictive silencing factor/repressor element silencing transcription factor, a neuron-restrictive silencer. 899 82

To investigate the frequency of pheochromocytoma in patients with incidentally discovered adrenal masses (incidentalomas) and to evaluate the sensitivity, specificity and diagnostic accuracy of the Glucagon test in comparison with resting plasma catecholamines, 89 patients with adrenal incidentalomas (age range 23-80 yr; 41 males and 48 females) were studied. Fifty-seven patients were normotensive (SBP 130+/-1.8 mmHg; DBP 80+/-0.7 mmHg, mean+/-SE) and 32 had stable hypertension (SBP 155+/-3.3 mmHg, DBP 93+/-1.4 mmHg): no patient complained of typical signs or symptoms of pheochromocytoma. Resting plasma samples for noradrenaline and adrenaline determination and, at appropriate intervals, the Glucagon test (1 mg i.v.), were performed in all subjects. Diagnosis of pheochromocytoma was made on the basis of humoral evaluations and/or surgical intervention in 6 patients (6.7%), of whom 3 hypertensives and 3 normotensives. Resting plasma catecholamines revealed 5 out of 6 patients with pheochromocytoma: in 3 cases both catecholamines were above the normal range, in 1 only adrenaline was elevated and in 1 case only noradrenaline. Similarily, the glucagon test identified 5/6 pheochromocytomas: in 3 patients the response was abnormal for both catecholamines, in 1 only for adrenaline and in 1 case only for noradrenaline. The sensitivity, specificity, and diagnostic accuracy of resting plasma catecholamines and of the glucagon test were comparable: 83.3%, 96.3%, and 95.5%, respectively. In conclusion, the frequency of pheochromocytoma in adrenal incidentalomas is not negligible, and since the diagnostic accuracy of the Glucagon test is the same of that of resting plasma catecholamines, the former does not appear to offer additional advantages in the diagnosis of incidentally discovered pheochromocytomas.
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PMID:Frequency of pheochromocytoma in adrenal incidentalomas and utility of the glucagon test for the diagnosis. 912 85


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