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)

The clinical significance of the direct determination of plasma ACTH was investigated in healthy persons and in patients with primary or secondary adrenocortical insufficiency, with Cushing's syndrome or with acromegaly. The sensitivity of the radioimmunological method facilitated the detection of diurnal changes in plasma ACTH in healthy subjects and of variations in plasma ACTH after the administration of dexamethasone and glucagon. The determination of plasma ACTH appears to be a useful procedure of diagnostic value in patients suffering from primary adrenal insufficiency accompanied by high concentrations of plasma ACTH. However, in patients suffering from Cushing's syndrome or secondary adrenocortical insufficiency it is still essential to carry out the dexamethasone suppression test or the metopiron test, respectively.
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PMID:[The clinical significance of the radioimmunological determination of plasma ACTH (author's transl)]. 18 Jun 98

The adenylate cyclase responses of the human GH or ACTH producing pituitary adenomas and ectopic ACTH producing tumors to TRH, LH-RH, biogenic amines, peptides hormones, PGE1 and rat median eminence extract (MEE) have been examined. Out of 4 GH producing pituitary adenomas obtained from patients with active acromegaly at hypophysectomy two were stimulated by TRH, two by LH-RH, three by norepinephrine, one by dopamine, four by PGE1 and none by serotonin. Glucagon stimulated the adenylate cyclase in one of three and MEE in both of two tested. The positive responses of paradoxical GH release after TRH and/or LH-RH before surgery in these patients coincidentally related to the response of adenylate cyclase of each pituitary adenoma. There seems, however, to be no consistent correlation between the adenylate cyclase responses to biogenic amines and the GH release after L-Dopa or 5-hydroxytroptophan tested. The adenylate cyclase of a pituitary adenoma from case of Cushing's disease was stimulated by LH-RH, norepinephrine glucagon and MEE but not by TRH. Plasma levels of ACTH, beta-MSH and cortisol increased after LH-RH but not after TRH in this patient before hypophysectomy. The adenylate cyclase of two ectopic ACTH producing tumors (gastric carcinoid and malignant thymoma) was activated by TRH, LH-RH, norepinephrine, epinephrine, serotonin, PGE1 and MEE. These results indicate the presence of multiple hormone receptors in GH or ACTH producing pituitary adenomas and ectopic ACTH producing tumors, and suggest that the paradoxical GH or ACTH release after TRH and/or LH-RH injection in acromegaly and Cushing's syndrome might be caused by an alteration of the cellular membrane receptors of the pituitary adenomas.
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PMID:Adenylate cyclase of GH and ACTH producing tumors of human: activation by non-specific hormones and other bioactive substances. 19 Feb 56

24 diabetics, (9 thin diabetics, 14 cases of maturity onset diabetes, 6 intermediate forms and one case of partial pancreatectomy) received 7.5 to 20 mg of bromocriptine (CB 154) per 24 hours. A definite improvement in glucose metabolism was noted in 6 cases, a definite aggravation in 4 cases; 14 results were not significant (p-0.05). The efficacy of CB 154 did not depend on the clinical type nor on the patient's age. It appeared related to duration of the diabetes (2 years and 3 months in improved patients, 11 years in aggravated patients) and perhaps the degree of retinopathy (more frequent and severe in aggravated patients). The improvement seems to be linked to the existence in certain diabetics of a paradoxical regulation of STH secretion as in acromegaly. The possibility of a peripheral effect of bromocriptine on insulin and glucagon is discussed. The CB 154 test (estimations of STH after a single dose of 2.5 mg) permits one to foresee the efficacy of the drug and perhaps the risk of diabetic retinopathy.
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PMID:[Action of bromocriptine on glucose metabolism in diabetics]. 20 Oct 30

Plasma glucagon levels were determined after 50 g of oral glucose loading in eleven acromegalics and fourteen normal subjects. Basal plasma glucagon levels were significantly elevated in patients with acromegaly, as compared with those in normal subjects. Oral glucose loading caused a decrease in plasma glucagon in normal subjects but not in acromegalics. Since this non-suppressibility of plasma glucagon by orally administered glucose was observed even in acromegalics without diabetes, it is concluded that insensitivity of the pancreatic alpha cell to hyperglycaemia exists in patients with acromegaly as well as in diabetics.
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PMID:Acromegaly: insensitivity of the pancreatic alpha cell to hyperglycaemia. 37 62

In 7 acromegalic patients growth hormone responses were studied following administration of synthetic TRF, propranolol-glucagon, insulin, and glucose p.o. Except for the glucose tolerance test, a good reproducibility of the STH response was observed. In 5 out of the 7 patients, there was a distinct rise in the plasma STH level after TRF. All patients with a positive insulin tolerance test responded to TRF, as did the two late responders to glucagon; the early responder to the latter test did not respond to TRF. It has been suggested (Liuzzi et al. 1974a) that TRF might be used as a screening test for detecting hypothalamic dependency of the acromegaly. This study suggests that further study is required before accepting this hypothesis and that a response to a combination of tests (TRF, glucagon, insulin) might be a better screening method.
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PMID:Comparison of TRF, propranolol-glucagon, insulin and glucose stimulation tests in acromegaly. 40 15

Changes in the serum level of growth hormone have been studied in 28 diabetics (6 exhibiting no diabetic retinopathy (d. r.), 10 displaying a non proliferative d. r., 6 having proliferative d. r., and 6 Brittle-diabetes) together with a control group consisting of 11 subjects (5 being totally healthy, and 6 having acromegaly without d. r.). Blood samples were obtained before and after arginine and glucagon administration and also following controlled exercise on the ergometer with 50% of the actual working capacity during 20 minutes. The presence of d. r. and its stage has been determined by fluorescein angiography. Our results demonstrate that an increased secretion of growth hormone in diabetics actually constitutes a manifestation of metabolic instability. Apparantly no correlation exists between the appearance of d. r. or its stage and the degree of growth hormone release.
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PMID:[Growth hormone and diabetic retinopathy (author's transl)]. 63 68

Plasma glucagon and insulin responses to L-arginine were compared in normal controls and patients with isolated growth hormone deficiency and acromegaly. Patients with isolated growth hormone deficiency were characterized by high plasma glucagon response and low plasma insulin response, whereas acromegalic patients showed exaggerated plasma glucagon response and almost normal insulin response. These results suggest that growth hormone is probably required for optimum function of the islets, and since hyperglucagonaemia was observed in both growth hormone deficiency and acromegaly, metabolic disturbances stemming from the respective primary diseases may affect glucagon secretion.
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PMID:Growth hormone modulation of arginine-induced glucagon release: studies of isolated growth hormone deficiency and acromegaly. 74 97

Somatostatine is the hypothalamic factor which inhibits the secretion of growth hormone. The administration of a synthetic form decreased growth hormone levels by 50 to 75% in 5 acromegalic patients. The action is rapid but the effect is not prolonged. Prolactin was reduced in only case with galactorrhea. Thyreostimulin, as well as gastrin, are unaffected. Plasma insulin levels, and to a lesser extent those of glucagon, are decreased by somatostatine which causes no variation in either cortisol or blood glucose. Somatostatine, by correcting the pathological secretion of hormone, opens the way to medical treatment of acromegaly.
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PMID:[The effects of somatostatin in acromegaly]. 77 91

Glucagon is secreted not only by A2-cells of the pancreatic islets but also by A cells in the gastric fundus and duodenum. Several reports have demonstrated that the glucagon plasma concentration is increased in genetic diabetes as well as in many conditions associated with a decreased glucose tolerance such as hepatic cirrhosis, myocardial infarction, infectious diseases, burns, taumatic shock, glucagonomas, acute pancreatitis, acromegaly, pheochromacytoma and Cushing's syndrome. Hyperglucagonemia is particularly important in diabetic ketoacidosis and in non-ketotic hyperosmolar coma. The mechanisms responsible for the diabetic's hyperglucagonemia remain controversial. According to several authors, the increased glucagon secretion is, for its main part, secondary to a prolonged defect in insulin secretion and thus relatively insensitive to an acute insulin administration. According to others, the A cell abnormality is of primary origin, independant from insulin deficiency and its effects are cumulative with those of the insulin lack. Several reports dealing with induced or spontaneous experimental diabetes are in favor of the first or the second hypothesis. It appears likely that glucagon plays a role in the metabolic derangments of diabetes. Indeed, hepatic glucose production is closely related to the ratio of molar concentrations of insulin and glucagon. Finally, in insulin-dependant diabetics, somatostatin infusion reduces plasma glucagon concentration and blood glucose and prevents the development of ketosis after withdrawal of insulin therapy. These results illustrate the contribution of glucagon in the pathogenesis of hyperglycemia and ketosis. Several arguments have been accumulated in favor of the following concept: diabetes hyperglycemia results both from glucose under-utilization secondary to insulin lack and from hepatic glucose over-production due to glucagon excess. Although controversial, the role of glucagon in ketogenesis appears likely.
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PMID:[The role of glucagon in hyperglycemia. A review (author's transl)]. 79 28

Growth hormone (GH) responses to L-dopa, 2-Br-alpha-ergocryptine (CB-154), thyrotropine-releasing hormone (TRH), luteinizing hormone-releasing hormone (LH-RH), glucagon and glucose were investigated in six patients with active acromegaly. The following results were obtained. 1) Subcutaneous injection of 1 mg glucagon caused a clear-cut decrease in plasma GH levels in 5 out of 6 active acromegalic patients at 30 minutes after the injection. In 2 out of 6 patients a rebound of plasma GH was observed. 2) In three out of six patients with active acromegaly, oral administration of 0.5 g L-dopa caused a significant suppression of plasma GH levels. 3) CB-154 (2.5mg) administered orally elicited a marked decrease in plasma GH levels in the same three patients who showed a significant suppressive GH reponse to L-dopa, and the inhibitory effect of CB-154 on GH secretion lasted for 6 hours. These patients who had a GH response to L-dopa or CB-154 were named "responders". 4) Intravenous administration of TRH resulted in a significant increase in plasma GH in 4 patients 3 of whom were responders and the other a non-responder. 5) Pretreatment with CB-154 did not modify the TRH-induced GH increase in all patients who had a positive response to TRH. 6) A significant increase in plasma GH was elicited by the intravenous injection of 100 mug LH-RH in 3 out of 6 patients with acromegaly. 7) When oral administration of CB-154 had been given 2 hours before LH-RH, the GH response to LH-RH was blunted in two of three patients who had a LH-RH-induced increase in plasma GH levels.
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PMID:[Comparison with growth hormone responses to various drugs or substances in patients with active acromegaly (author's transl)]. 82 92


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