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)

Glucagon activated adenylate cyclase in a homogenate of a pheochromocytoma over the concentration range 1 times 10 minus 8M to 1 times 10 minus 6M. Several other hormones including adrenocorticotropin, thyrotropin, parathyroid hormone and histamine were without effect. The tumor glucagon receptor was characterized and found to be similar in several ways to the glucagon receptor previously reported in normal tissue such as liver and heart. One, the receptor specifically bound 125-I-glucagon. Two, solubilization of the pheochromocytoma abolished glucagon-activation of the adenylate cyclase. Three, glucagon-responsiveness of the adenylate cyclase was partially restored by the addition of phosphatidylserine to the incubations. One major difference was observed between the glucagon receptor in tumor tissue and that in liver and heart, namely, a marked lability in 125-I-glucagon binding and adenylate cyclase activity. Within four days, despite storage in liquid nitrogen, 75% of the binding activity and all of the adenylate cyclase activity in the solubilized preparation were lost. The factor(s) responsible for this lability remains unidentified.
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PMID:Characterization of the glucagon receptor in a pheochromocytoma. 16 16

Arginine infusion tests were carried out in seven patients with pheochromocytoma before and after extirpation of the tumors in order to evaluate pancreatic islet alpha- and beta-cell function during the state of endogenous catecholamine excess. Six of the patients had glucose intolerance; one did not. Preoperatively, the pancreatic glucagon response was suppressed, while the insulin response was comparable to that in normal control subjects. Plasma glucose levels decreased rapidly after the beginning of arginine infusion in all patients. Theses changes during the infusion were evident in the one patient without glucose intolerance. Postoperatively, the glucagon response and plasma glucose changes were normalized. In addition to the obvious suppression of pancreatic alpha-cell function in our patients with pheochromocytoma, it seems likely that pancreatic beta-cell function also was suppressed; there was no enhancement of the insulin response to arginine during the period of chronic hyperglycemia, a situation in which a synergistic effect between glucose and arginine might be expected.
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PMID:Pancreatic alpha- and beta-cell function in pheochromocytoma. 38 21

42 patients suspected of pheochromocytoma underwent to sulpirid and glucagon tests. 6 patients had pheochromocytoma: 3 failed to respond to glucagon and 2 to sulpirid. The 36 other patients had no clinical or blood pressure changes after sulpirid injection. We did not know any complication in positive tests and any clinical unconfort in negative tests. These results confirm the interest of sulpirid test in pheochromocytoma.
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PMID:[Place of sulpirid test in the diagnosis of pheochromocytoma (author's transl)]. 54 79

In one female patient suffering from an extra-adrenal pheochromocytoma, a stimulation test with glucagon was performed. In spite of the absence of an increase in heart rate and blood pressure, a pronounced increase in plasma catecholamines showed this test to be positive. The authors discuss the reliability criteria of this test, and confirm its good tolerance.
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PMID:[Merits of the assay of plasma catecholamines in a glucagon test to diagnosis of pheochromocytoma (author's transl)]. 64 81

In 149 cases, blood pressure response to glucagon test did not exceed 20/10 mm Hg more than the response in the cold pressor test control and was considered negative. Plasma catecholamine level increases may be seen in 95% of patients without pheochromocytomas. Among six patients with pheochromocytomas, urinary metanephrine levels were of diagnostic importance in two with isolated pheochromocytoma and in one with the multiple endocrine neoplasia of type 2 (MEN-type 2). Urinary metanephrine determinations yielded false-negative results in three patients with MEN-type 2, while vanilmandelic acid level was normal in one and nephrotomograms were positive in two of these three. These results suggest that the early diagnosis of pheochromocytoma in patients with MEN-type 2 may be difficult and may require multiple biochemical and roentgenographic investigations.
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PMID:Glucagon-blood catecholamine test: use in isolated and familial pheochromocytoma. 116 24

We have evaluated intravenous glucagon as pharmacologic stimulus to adrenal catecholamine secretion in normal human subjects. Urinary epinephrine and norepinephrine were measured at two hourly intervals before and after the intravenous injection of saline, 4 mg glucagon, or 0.1 mu/kg crystalline insulin. Urinary epinephrine was increased 2.3-fold over baseline after both saline and glucagon. By contrast, insulin hypoglycemia produced a 24-fold rise in urinary epinephrine. No rise in urinary norepinephrine was detected in any test. Under the conditions of this study, we conclude that epinephrine excreted after glucagon injection is due to the stress of the test itself. In normal man, glucagon either does not stimulate adrenal catecholamine secretion, or the effect is too small to measure. By contrast, in pheochromocytoma, glucagon may be specific for catecholamine secretion, based on data from the literature. In normal subjects, insulin hypoglycemia remains the only proved method for assessing adrenal catecholamine reserve.
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PMID:Effect of intravenous glucagon on urinary catecholamine excretion in normal man. 125 Jan 59

A 45-year-old hypertensive female with insulin-treated diabetes mellitus presented to our clinic with elevated urinary norepinephrine (NE) concentrations and a negative 131-metaiodobenzylguanidine (MIBG) scintigraphy, errouneously limited to the abdomen, for evaluation of a pheochromocytoma (Pheo). Despite antihypertensive medications blood pressure remained highly variable and frequently elevated. Further biochemical testing, including a glucagon provocation test and a clonidine-suppression test, revealed autonomous NE secretion. In order to avoid repeat MIBG-scintigraphy, other non invasive imaging techniques were performed, including real time sonography (7.5 MHz) of the neck which revealed a tumor. Fine needle aspiration of this tumor tissue demonstrated cells compatible with Pheo. Histology and immunohistochemistry of the excised tumor confirmed the diagnosis of Pheo. After surgical removal of the tumor, urinary and plasma NE levels normalized. Without any medication the blood pressure of the patient was now only slightly hypertensive. Only half of the daily insulin dose was needed to maintain the patient euglycemic.
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PMID:Cervical pheochromocytoma: a rare localization and a difficult diagnosis. 149 Nov 26

The present study investigated whether in vivo endogenous opioids inhibit the secretory activity of pheochromocytomas and whether opioid antagonists may be useful in the diagnosis of pheochromocytoma. In six patients with pheochromocytoma in whom the diagnosis was histologically confirmed after surgery, mean intraarterial blood pressure (BP) increased by 45 mm Hg within 3 min after intravenous (i.v.) injection of 2 mg glucagon (95% confidence interval 23-68 mm Hg); heart rate (HR) remained unchanged, whereas plasma norepinephrine (NE) increased by 216% (31-658%) and plasma epinephrine (EPI) increased by 203% (37-571%). Although glucagon stimulation confirmed the secretory potential of the pheochromocytomas, opioid antagonism by a 10-mg i.v. bolus of naloxone produced no significant change in plasma NE and EPI concentrations or intraarterial pressure. The present study does not support the hypothesis that release of catecholamines from pheochromocytomas is inhibited by endogenous opioids. Use of opioid antagonists as a tool in the diagnosis of pheochromocytoma therefore cannot be recommended.
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PMID:Influence of opioid antagonism on plasma catecholamines in pheochromocytoma patients. 169 61

We assessed the sensitivity and specificity of glucagon stimulation and clonidine suppression tests in the diagnosis of pheochromocytoma in 113 hypertensive patients, 39 with and 74 without the tumor. In the glucagon stimulation test, blood was sampled 2 minutes after intravenous injection of 0.28 mumol (1 mg) glucagon, and in the clonidine suppression test, blood was sampled 3 hours after administration of oral clonidine, 1.30 mumol (0.3 mg)/70 kg body wt. Baseline levels of catechols in antecubital venous blood were abnormal, with norepinephrine greater than 7.10 nmol/l (1,200 pg/m), epinephrine greater than 1.51 nmol/l (276 pg/ml), norepinephrine/dihydroxyphenylglycol (DHPG) ratio greater than 1.09, or dopa greater than 35.53 nmol/l (7,000 pg/ml), in 30 of 39 patients with pheochromocytoma (sensitivity 77%) and 1 of 74 patients without pheochromocytoma (specificity 99%). Results of the glucagon test were abnormal (norepinephrine greater than 11.83 nmol/l [2,000 pg/ml] or more than threefold increase from baseline) in 25 of 31 patients with pheochromocytoma (sensitivity 81%) and 0 of 72 patients without pheochromocytoma (specificity 100%). Results of the clonidine test were abnormal (after clonidine norepinephrine greater than 2.96 nmol/l [500 pg/ml] or less than 50% decrease from baseline) in 29 of 30 patients with pheochromocytoma (sensitivity 97%) and in 7 of 30 patients without pheochromocytoma (specificity 67%). Very high baseline levels of catechols therefore indicated the presence of pheochromocytoma, but there were several false-negative results when normal levels were obtained. The glucagon test alone was highly specific but not sensitive, and the clonidine test was highly sensitive but less specific.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Glucagon and clonidine testing in the diagnosis of pheochromocytoma. 204 33

In six patients with pheochromocytoma oral glucose tolerance test (OGTT) and arginine test were carried out. Blood insulin and glucagon response were investigated. In subjects with adrenal tumor glycemic curve pattern was typical: a rapid and exaggerated increase of glycemia followed by an abrupt drop. Absolute insulinemic response to oral glucose was normal, but inappropriate to glycemic stimulus. Arginine infusion provoked a slightly above normal increase in blood glucose and a normal increase in blood glucagon. In three of the patients studied postoperatively, reduced glycemic response to glucose was observed, whereas there were no evident variations in blood insulin and glucagon response. These data suggest that in pheochromocytoma impaired glucose tolerance is partly due to the reduced insulin response to oral glucose load.
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PMID:Endocrine pancreatic function in pheochromocytoma. 207 24


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