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)

Unstable diabetes is characterized by the appearance of irregular and unpredictable variations of the glycemia; because of this it is very difficult to achieve an acceptable metabolic control. There are different criteria (continuous monitorization, M value, MDDG, AMEG, etc.) for the evaluation of the degree of instability. Unstable diabetes may be transitory (generally related to exogenous factors or erroneous management) or permanent. The Somogyi effect must always be taken into account in unstable diabetes. The two most important pathogenic factors could be the absence of the pancreatic insulin reserve and the presence of small quantity of anti-insulin antibodies of high affinity. Other factors such as glucagon, growth hormone, catecholamines, etc. seem to play a secondary role. At the moment the treatment of unstable diabetes is not very satisfactory.
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PMID:[Unstable diabetes (author's transl)]. 52 31

1. A new line of cloned, differentiated rat hepatocytes (RL-PR-C) was evaluated for its usefulness as an in vitro system for studying the regulation of the insulin receptor. 2. Insulin rapidly reversibly and specifically bound to RL-PR-C hepatocytes. Binding of tracer 125I-labeled insulin, which was competitively inhibited by native insulin as well as by proinsulin and analogs of insulin and proinsulin in proportion to their biological activity, was not influenced by glucagon, corticotropin, or human growth hormone. Anti-insulin receptor serum from a patient with Acanthosis Nigricans Type B competed with 125I-labeled insulin for binding to cell surface sites. 3. Trypsinization destroyed insulin binding sites, but these were restored by incubation under growth conditions; a 75% restoration of binding sites was achieved by one cell population doubling. 4. RL-PR-C hepatocytes responded to insulin binding by an increase in glycogen synthesis from glucose. The insulin effect was maximal at 85 nM, but was detectable at lower, more physiological, concentrations. 5. Chronic exposure (for at least 3h) of hepatocytes to insulin (10(-10)--(10(-8) M) reduced by up to 60% the number of binding sites for insulin (down-regulation). Down-regulation was prevented by cycloheximide at concentration (10 micron) sufficient to inhibit markedly protein synthesis from tracer isoleucine. Recovery from down-regulation induced by native insulin at 10(-7 M or lower concentrations was complete by 18 h under growth conditions. 6. Although RL-PR-C hepatocytes spontaneously transform after about 90 population doublings, no significant differences between normal and transformed cells were observed in insulin binding characteristics and in interaction of cells with anti-insulin receptor serum. However, transformed cells exhibited a substantially reduced (maximum of 20%) down-regulation response to insulin. 7. RL-PR-C rat hepatocytes appear, for these reasons, to be a useful model system for studying the regulation of the insulin receptor.
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PMID:Hormone receptors. 7. Characteristics of insulin receptors in a new line of cloned neonatal rat hepatocytes. 56 93

A propranolol-glucagon test was evaluated in 24 control normal children, 21 pituitary dwarfs, 15 patients with constitutional short stature, 2 with chromosome aberration and 4 with miscellaneous diseases. The dose of glucagon enough for the stimulation of human growth hormone (HGH) secretion is more than 20 microgram/kg of body weight. During the test in the control subjects the serum HGH level increased from 2.3 +/- 1.2 ng/ml to a maximum level of 30.0 +/- 15.1 ng/ml, when 10 mg propranolol, regardless of body weight and 30 microgram glucagon per kg of body weight are given. The dose of propranolol administered ranged from 0.2 to 1.0 mg/kg of body weight in normal children studied. Serum 11-OHCS also increased significantly from 14.5 +/- 11.2 microgram/100 ml to 30.1 +/- 15.5 microgram/100 ml (P less than 0.01). There was no difference in the maximum level of urinary total catecholamines in propranolol-glucagon test between 7 pituitary dwarfs and 7 control subjects. The mechanism of HGH response to propranolol-glucagon administration is unknown, but propranolol-glucagon administration is a sensitive and reliable provocative test for HGH secretion, since false negative response of HGH are not observed in patients with non-pituitary disease.
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PMID:Evaluation of propranolol-glucagon test. 57 17

Administration of a low-dose insulin infusion to normal subjects results in a mild drop in blood glucose concentration (1.1 mmol/1 (20 mg/100 ml)) and the resetting of the basal glucose at the lower concentration. Clinical hypoglycaemia does not develop, and there is a significant release of glucagon, growth hormone, and cortisol. A similar infusion in insulin-requiring diabetics results in hypoglycaemia accompanied by a release of growth hormone and cortisol but no significant release of glucagon. Subsequently giving arginine to these patients results in a significant release of glucagon, indicating that the alpha cell is intact and can respond to local, direct stimulation. In one patient the defect in glucagon response to impending hypoglycaemia developed after two years' insulin treatment. This type of dissociated response' of the alpha cell has been reported in animals after denervation of the pancreas, and insulin-requiring diabetics may develop a selective form of autonomic neuropathy affecting the vagal control of glucagon release.
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PMID:Defective blood glucose counter-regulation in diabetics is a selective form of autonomic neuropathy. 58 16

In 6 normal subjects, L-dopa (500 mg PO) and apomorphine (0.6 mg sc) increased circulating growth hormone and suppressed prolactin levels in a parallel and quantitatively similar fashion, but only L-dopa induced a rise in plasma glucagon, glucose, and insulin levels. The failure of apomorphine to affect glucagon secretion, despite a substantial effect on growth hormone and prolactin, was also observed in insulin-dependent diabetics known to exhibit A-cell hyperresponsiveness to various stimuli. In view of the highly dissimilar molecular and pharmacologic characteristics of L-dopa and apomorphine, these data do not exclude a local dopaminergic effect of L-dopa at the pancreatic level, but strongly militate against a central dopaminergic pathway for glucagon stimulation.
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PMID:Differential effects of L-dopa and apomorphine on glucagon secretion in man: evidence against central dopaminergic stimulation of glucagon. 59 12

Hormone effects on the synthesis of alpha(1) (acute-phase) glycoprotein and of albumin by isolated rat hepatocytes in suspension were examined. Insulin, glucagon, cortisol, somatotropin (bovine growth hormone) and tri-iodothyronine were added to achieve physiological concentrations in the medium [Jeejeebhoy, Ho, Greenberg, Phillips, Bruce-Robertson & Sodtke (1975) Biochem. J.146, 141-155]. After periodic additions, there were increases (compared with values for non-hormone-treated suspensions) in the concurrent absolute syntheses of alpha(1) (acute-phase) glycoprotein and of albumin. Trends were detectable after 24h, and significant increases were demonstrated after 48h of incubation (219 and 119% respectively of control values). Manipulation of hormones, by omission from the mixture or by addition of only one or two hormones in various combinations, indicated that for alpha(1) (acute-phase) glycoprotein (which may be representative of some other acute-phase proteins), cortisol was one of the most important hormones involved in the stimulation of synthesis, with glucagon enhancing the effect of cortisol but not being stimulatory by itself. Addition of actinomycin D inhibited this stimulation, suggesting that cortisol might have acted through promotion of RNA synthesis. For albumin, cortisol alone did not stimulate synthesis, but its absence from a hormone mixture significantly decreased synthesis compared with that observed with the complete hormone mixture. Our findings support the possibility that following tissue injury, synthesis of alpha(1) (acute-phase) glycoprotein may be stimulated by the hormonal response to this injury (which response includes elevated blood concentrations of cortisol and glucagon).
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PMID:Effects of hormones on the synthesis of alpha 1 (acute-phase) glycoprotein in isolated rat hepatocytes. 60 39

Carbohydrate intolerance is a common abnormality in patients with chronic renal failure. In this group of patients we investigated the interrelation among glucose, insulin, and growth hormone and confirmed the presence of carbohydrate intolerance and hyperinsulinemia. In addition we demonstrated alterations in growth hormone regulation, characterized by (1) the lack of suppression of growth hormone by orally induced hyperglycemia and paradoxical increase in serum levels of growth hormone after the administration of intravenous glucose or glucagon; (2) lack of release of growth hormone with induced hypoglycemia and an exaggerated response to levodopa administration. Furthermore, thyrotrophin-releasing hormone stimulated growth hormone release, a phenomenon not observed in the control population. Our studies show an impaired hypothalamic regulation of growth hormones secretion in patients with renal failure undergoing long-term hemodialysis.
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PMID:Abnormalities in the regulation of growth hormone in chronic renal failure. 62 54

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

In the course of familial idiopathic haemochromatosis with diabetes, after stimulation with arginine, the alpha cell responds perfectly to stimulation, in contrast to the case of chronic pancreatic diseases. After an oral glucose load, there is no reduction in plasma glucagon concentrations, and a paradoxal increase is sometimes seen. These results are quite similar to those reported in common diabetes. Secretion of growth hormone after an infusion of arginine and insulin hypoglycaemia seem to be significantly reduced in comparison with normal subjects and those suffering from common diabetes, paired and explored using the same protocol. This may perhaps explain the low degree of severity and slow course of associated vascular disease.
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PMID:[Familial idiopathic haemochromatosis with diabetes. Study of glucagon and growth hormone secretions (author's transl)]. 63 72

Somatostatin was infused in various doses into normal subjects and juvenile diabetics for a 24-hour period preceded by a 24-hour control period and followed by another three-hour control period. Saline was infused during the first control period. Meals were served during the two 24-hour periods. Blood samples were taken hourly. Five normal males received a total dose of 4 mg. somatostatin. Four male diabetics received 2 mg., four received 4 mg., and four 6 mg. In the diabetics, somatostatin suppressed plasma growth hormone, glucagon, and glucose throughout the infusion. All parameters rebounded at cessation of infusion. In the normals, somatostatin suppressed plasma growth hormone, glucagon, and insulin but increased plasma glucose. It is concluded that the plasma glucose suppression in the diabetics is mainly due to the suppression of the diabetogenic hormones growth hormone and glucagon. A minor effect of decreased and/or delayed absorption of carbohydrates cannot be excluded in these experiments. The elevated plasma glucose levels in normals must be due to the suppressive effects of somatostatin on insulin secretion.
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PMID:24-hour studies of the effects of somatostatin on the levels of plasma growth hormone, glucagon, and glucose in normal subjects and juvenile diabetics. 64 Feb 35


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