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)

Immunoreactive plasma glucagon (IRG) in normal subjects and patients with chronic renal failure, diabetic ketoacidosis and diagetic hyperosmolar syndrome circulates in several forms. In the diabetic patients most IRG eluted coincidentally with the extracted, purified pancreatic hormone (MW3500), while in normal subjects a high molecular weight component predominated. In striking contrast, the major component of plasma IRG in patients with chronic renal failure was of intermediate size (MW +/- 9000), consistent with proglucagon. The accumulation of this form of IRG suggests that the kidney plays an important role in its metabolism. If there are differences in the biological activity of the various circulating components of IRG, the significance of immunoreactive glucagon levels in some disease states will require reassessment.
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PMID:Heterogeneity of plasma glucagon: patterns in patients with chronic renal failure and diabetes. 124 85

To establish a qualitative and quantitative model of blood glucose response to stress hormone exposure, healthy subjects (HS) on and off somatostatin (250 micrograms/h) as well as insulin dependent diabetic patients were infused with either epinephrine (E), glucagon (G), cortisol (F), growth hormone (GH) or with a cocktail of these hormones raising plasma stress hormones to values seen in severe diabetic ketoacidosis. The developed input/output model consists of two submodels interconnected in series plus two additional submodels for correction of gains describing both sensitivity of tissue response and utilisation as well as provision of glucose. It was shown and confirmed experimentally that blood glucose response to stress hormones was essentially nonlinear. Furthermore, the mathematical models for healthy subjects and for insulin dependent diabetic patients proved to be of the same structure and differed only in the values of some typical parameters. The model raises the possibility to describe and in part to predict blood glucose response to stress hormone exposure in healthy man and insulin dependent diabetic patients.
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PMID:Blood glucose response to stress hormone exposure in healthy man and insulin dependent diabetic patients: prediction by computer modeling. 135 49

1. Exogenous somatostatin inhibits glucagon secretion and prevents ketoacidosis in diabetic patients, but has the therapeutic disadvantage of requiring continuous intravenous infusion to exhibit these effects. 2. Consequently, we examined the effect of subcutaneous administration of the long-acting somatostatin analogue octreotide (SMS 201-995) on early ketogenesis in diabetic ketoacidosis. On two separate occasions insulin was withdrawn over a period of 9 h from seven type I diabetic patients. On the second occasion the patients were given 50 micrograms octreotide s.c. before the insulin withdrawal and every 3 h during insulin withdrawal. 3. Differences in integrated free fatty acid responses (4706 +/- 1227 mumol l-1 h vs 3026 +/- 835 mumol l-1 h, AUC, P = NS) were not significant, but the peak increments of acetoacetate (1413 +/- 354 mumol l-1 vs 612 +/- 176 mumol l-1, P less than 0.05), beta-hydroxybutyrate (2180 +/- 475 mumol l-1 vs 922 +/- 246 mumol l-1, P less than 0.01) and the decrements in plasma bicarbonate (-8 +/- 1 mumol l-1 vs -4 +/- 1 mumol l-1, P less than 0.05) and pH (-0.07 +/- 0.01 vs -0.03 +/- 0.01, P less than 0.05) were significantly less with octreotide. 4. At the same time peak increments of glucagon were lower with octreotide treatment (329 +/- 206 pg ml-1 vs 39 +/- 30 pg ml-1, P less than 0.05). 5. We conclude that, despite accelerated lipolysis and provision of substrate for ketogenesis during insulin withdrawal, this somatostatin analogue significantly reduces ketogenesis resulting from insulin deprivation, probably secondary to decreasing glucagon secretion. This drug may be useful in short term prophylactic treatment of diabetic patients during periods of increased risk for ketoacidosis.
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PMID:Preventive effects of octreotide (SMS 201-995) on diabetic ketogenesis during insulin withdrawal. 195 71

Ketoacidosis, severe hyperosmolality due to hyperglycemia, and severe hypoglycemia are all life-threatening emergencies that often occur in the absence of any history of diabetes mellitus. The key to management of diabetic ketoacidosis is understanding that treatment is aimed more at the breakdown and metabolism of triglycerides in adipose tissue than at hyperglycemia per se. The diabetic hyperosmolar state is most easily treated with aggressive fluid management, with the caveat that too-rapid administration of hypotonic fluids may increase the already significant mortality from this condition. Life-threatening hypoglycemia most commonly occurs with administration of oral hypoglycemic drugs or insulin, although other drugs and any malnourished state may also be precipitating factors. Acute administration of glucagon or dextrose alleviates life-threatening hypoglycemia. Success in managing these diabetic emergencies depends on rapidity of recognition and institution of direct treatment measures.
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PMID:'Diabetic' emergencies. They happen with or without diabetes. 211 37

Hyperglucagonemia accompanies several disorders such as acute pancreatitis and diabetic ketoacidosis characterized by increased amylase/creatinine clearance ratio (ACCR). We tested the hypothesis that glucagon may be responsible for the augmental ACCR among diabetic and/or obese subjects. A constant glucagon infusion (15 ng/kg/min) was given to eight noninsulin-dependent diabetics and to eight obese subjects to attain glucagon levels comparable with those obtained during acute pancreatitis. The ACCR significantly increased from 0.9 +/- 0.1 to 1.5 +/- 0.1% (p less than 0.005) in both noninsulin-dependent diabetics and obese subjects, whereas among normal control subjects the ACCR increased from 0.84 +/- 0.8 to 1.3 +/- 0.14% (p less than 0.001). Because the increased values observed in either noninsulin-dependent diabetics or obese subjects are less than the ACCR values observed in acute pancreatitis or in diabetic ketoacidosis, the elevated ACCR in those conditions is only partially explained by the hyperglucagonemia.
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PMID:Amylase/creatinine clearance ratio response to hyperglucagonemia in diabetes and obesity. 243 Apr 51

Ketoacidosis is a metabolic alteration caused by absolute or relative insulin deficiency and oversecretion of glucagon. Prompt diagnosis and rapid initiation of treatment are mandatory to avoid the complications and fatal outcome. Reduction of plasma glucose to levels within acceptable limits, block of ketogenesis, re-establishment of hydroelectrolytic balance, correction of alterations of acido-base status are the most important goals in DKA treatment. However, all the corrections should be made slowly and under continuous control. Altered parameters must slope off very gradually to prevent dangerous hazards.
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PMID:Diabetic ketoacidosis in children. 250 40

A review is presented on the care of three diabetic emergencies: diabetic ketoacidosis (DKA), hypoglycemias and sick days. A treatment scheme, based on low-dose insulin regime and i.v. insulin administration is presented. Plenty of emphasis is laid on fluid and electrolyte therapy. It is stressed that the primary goal in the treatment of DKA is not to reduce blood glucose, but to correct the fluid and electrolyte deficit and by administering insulin to correct the metabolic acidosis and change catabolism into anabolism. The use of bicarbonate in severe DKA is discouraged, and the risk of cerebral edema as a complication of the treatment is stressed. A diabetic child being treated for DKA needs particularly love and care. The three categories of hyperglycemias, mild, moderate, and severe, are briefly reviewed. In severe hypoglycemia (hypoglycemic shock) the treatment is either i.m. glucagon or i.v. glucose. In acute illnesses the use of extra doses of regular insulin is emphasized, in order to prevent DKA.
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PMID:Care in diabetic emergencies. 251 60

The effects of 3-hydroxybutyrate (3-OHB) and hyperosmolarity on glucagon secretion were examined in the isolated perfused canine pancreas. When 3-OHB was infused for 15 min into the pancreas perfused with 2.8 mM glucose, 5 and 20 mM sodium 3-OHB inhibited it after a transient stimulation, whereas a similar transient stimulation was observed also by the infusion of 20 mM NaCl in a control experiment. The above inhibition was not observed under the perfusate condition of 5.5 mM glucose plus 10 mM arginine. When the isolated canine pancreas was perfused under the perfusate condition of acidosis (pH 7.1), ketoacidosis (pH 7.1 and 20 mM 3-OHB) or hyperosmolarity (+60 mOsm/kg with sucrose) throughout the experiment, the glucagon concentrations produced by 2.8 mM glucose under the ketoacidotic and hyperosmolar conditions, were less than half of those obtained under the standard condition. The insulin level was not influenced by the above perfusate conditions. These results suggest that 3-OHB inhibits glucagon secretion stimulated by glucopenia, but does not inhibit it stimulated by amino acids, and that hyperosmolarity inhibits glucagon secretion but does not inhibit insulin secretion. The pathophysiological significance of these results must be slight, considering the presence of hyperglucagonemia during prolonged starvation or diabetic ketoacidosis.
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PMID:Effects of 3-hydroxybutyrate and hyperosmolarity on glucagon release from isolated perfused canine pancreas. 268 20

High circulating levels of somatostatin (SRIF) were detected in a patient with a metastatic tumour after development of diabetic ketoacidosis (DKA). Fasting insulin and C-peptide levels were markedly suppressed, but plasma glucagon was not suppressed below normal. Progressive cachexia ensued; at autopsy a poorly differentiated non-small cell neuroendocrine carcinoma metastatic to liver was found. Small gallstones were noted. Electron microscopy of tumour tissue showed neurosecretory granules and tonofilament bundles. Immunohistochemical staining of tumour cells was diffusely positive for carcinoembryonic antigen, bombesin-like immunoreactivity, and calcitonin with focal immunoreactivity for SRIF, serotonin, neuron-specific enolase, chromogranin, and epithelial membrane antigen. Column chromatography of plasma and tumour extract revealed five or more peaks of material with SRIF-like immunoreactivity (SRIF-LI): predominantly SRIF-28 and intermediates in tumour extract, and SRIF-14 and an intermediate between SRIF-28 and SRIF-14 in plasma, DKA in this case of somatostatinoma syndrome may reflect differential effects of tumour production of larger molecular weight SRIF forms on insulin and glucagon secretion.
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PMID:Malignant somatostatinoma presenting with diabetic ketoacidosis. 282 97

The glucagon-C-peptide test was evaluated as a predictor of the requirement of insulin therapy in type 2 diabetes mellitus. Endogenous insulin secretory capacity was measured in a population of 150 insulin-treated adult diabetic patients by determining postprandial glucagon-stimulated plasma C-peptide concentration (Novo, antiserum M 1230). Eleven subjects with C-peptide levels above 1.0 nmol/l comprised the subgroup in which the previously started insulin therapy was discontinued. After an observation period of a week in hospital the metabolic control of the patients was followed in an outpatient clinic for twelve months. During the observation period one patient was managed on diet alone, eight subjects required oral hypoglycaemics agents and two required the reinstitution of insulin therapy. Mean fasting blood glucose and GHbA1 (glycosylated haemoglobin) of non-insulin dependent diabetics increased during the observation period (from 8.8 to 11.8 mmol/l, p less than 0.001, and from 12.2 to 14.1%, p less than 0.05, respectively). No significant changes were found in total or HDL-cholesterol or triglyceride levels. The findings demonstrate that the glucagon-C-peptide test can be used as an aid in judging whether the withdrawal of insulin may be considered without excessive risk of developing diabetic ketoacidosis. However, the test cannot be used as the only criterion when assessing the need for exogenous insulin in type 2 diabetes. Meticulous monitoring of blood glucose levels is necessary when insulin therapy is withdrawn, because diabetic patients with peripheral insulin resistance may not maintain satisfactory glycaemic control without exogenous insulin despite of high residual endogenous insulin secretion.
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PMID:Glucagon-C-peptide test as a measure of insulin requirement in type 2 diabetes: evaluation of stopping insulin therapy in eleven patients. 331 47


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