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)

Low-dose insulin infusion has recently been used to treat ketoacidosis. We have prospectively compared patients with ketoacidosis either treated with insulin infusion at the rate of 6 units per hour or with high-dose, intermittent subcutaneously administered insulin, with emphasis placed on the hormonal responses. Basal glucagon, cortisol, and growth hormone levels were elevated in both groups. Cortisol and growth hormone levels did not fall with therapy in either group but glucagon levels fell in parallel with glucose levels in both groups. There was no difference in the time taken for glucose levels to fall below 250 mg/100 ml between groups. Whereas both methods of therapy appeared to be equally effective, low-dose infusion had the advantages of ease of administration, a predictable, relatively linear rate of fall of glucose levels, and ability to be stopped abruptly in the event of hypoglycemia.
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PMID:Low-dose continuous insulin therapy for diabetic ketoacidosis. Prospective comparison with "conventional" insulin therapy. 41 34

New concepts concerning the pathogenesis and therapy of diabetic ketoacidosis are reviewed. The regulation of ketogenesis by intrahepatic enzymic processes and the roles of insulin deficiency or glucagon or other counterregulatory hormone excess are summarized. Major emphasis is placed on an analysis of the use of low-dose insulin regimens for the treatment of ketoacidosis. Most patients with diabetic ketoacidosis will respond to low-dose, hourly, intravenous or intramuscular regular insulin. Low doses of insulin are as effective as high doses and have fewer associated complications of hypoglycemia and hypokalemia. Phosphorus deficiency is common in diabetic ketoacidosis and hypophosphatemia usually becomes manifest within 4 to 12 h of institution of therapy. Phosphorus supplementation is now generally recommended to replete erythrocyte 2,3-diphosphoglycerate and improve oxygen delivery to tissues. Coexistent and biochemically significant lactic acidosis is a relatively infrequent complication of diabetic ketoacidosis and when present is usually due to underlying disorders associated with poor tissue perfusion.
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PMID:Diabetic ketoacidosis: new concepts and trends in pathogenesis and treatment. 41 52

Augmentation of insulin release after oral glucose by a gastrointestinal humoral mechanism is well accepted. The suggestion of a similar mechanism for suppression of glucagon release after oral glucose has not been previously tested. In this study, plasma glucagon levels have been estimated in five normal subjects after both oral and iv administration of glucose. A variable iv glucose infusion rate with frequent monitoring of blood glucose was used to match the hyperglycemia produced by the 50 g oral glucose and the iv glucose loads. Virtually complete suppression of plasma glucagon levels was seen in both cases (nadir of glucagon levels 16 +/- 6 pg/ml for oral glucose; 11.4 +/- 3 pg/ml for iv glucose). Thus, enteric humoral factors did not facilitate glucagon suppression after oral glucose ingestion in man. The vagus nerve is also involved in mediating the alpha-cell response to hypoglycemia and, thus, to examine whether hyperglycemia suppresses glucagon release through a vagal mechanism, iv atropine (15 microgram/kg) was given 20 min before administration of oral or iv glucose. Atropinization delayed the glucagon suppression after oral glucose, but this delay was probably related to delayed glucose absorption from the gut. With iv glucose, atropinization did not affect the degree of suppression of glucagon levels. It is concluded that alpha-cell suppression in response to hyperglycemia is not mediated via the vagus.
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PMID:Hyperglycemia and glucagon suppression: possible importance of the vagus and enteric humoral factors. 42 94

The administration of cyproheptadine (25 mg/kg; i.p.) resulted in an increase of plasma insulin and glucagon (measured using 30 K antibody) 30, 60 and 120 min after injection to fasted rats. This dose of cyproheptadine also induced a hyperglycemia whereas a lower dose (5 mg/kg; i.p.), which did not alter plasma hormone levels, was associated with a hypoglycemia. Fed rats showed a reduction of plasma insulin with a similar elevation of blood glucose after cyproheptadine. Administration of an exogenous load of arginine resulted in increases of plasma insulin and glucagon of a greater magnitude than induced by cyproheptadine, however, cyproheptadine pretreatment (25 mg/kg) completely suppressed the pancreatic response to the amino acid, resulting in blood hormone levels similar to values seen after cyproheptadine administered alone. Cyproheptadine pretreatment also prevented the hyperinsulinemia and hypoglucagonemia resulting from glucose loading. alpha-Adrenergic receptor blockade (with phentolamine), beta adrenergic receptor blockade (with propranolol) and adrenodemedullation did not alter pancreatic responsiveness to the drug.
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PMID:Paradoxical short-term effects of cyproheptadine on insulin and glucagon release in the rat. 43 34

A substance present in the sera of diabetic children that interferes with the radioimmunoassay for glucagon was found in six of 66 children who were participating in an inpatient study of diabetic control. Detailed studies documented unequivocally that this glucagon-binding substance is a specific antibody to glucagon and is located in the immunoglobulins. In a survey of diabetic children in the outpatient diabetes clinic and in a diabetes summer camp, antibodies to glucagon were found in about 12% of those evaluated. However, no children who had had diabetes for less than three years were found to have antibodies, and there appeared to be an increase with increasing duration of disease of up to greater than 20% at eight years' duration. The presence of glucagon antibodies may be of pathologic significance in that the patients have a greater tendency to develop hypoglycemia than do diabetic children without glucagon antibodies.
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PMID:Circulating glucagon antibodies in children who have insulin-dependent diabetes mellitus. Clinical significance and characterization. 43 68

Continuous, low dose, insulin infusion in conscious dogs produced moderate hypoglycemia but only a transient fall in glucose production that rose towards preinfusion levels 20 to 30 min before any detectable increase in plasma counterregulatory hormones. Addition of epinephrine or glucagon to the insulin infusion prevented the fall in glucose production throughout the experiment but only partially diminished the hypoglycemic response. When hypoglycemia was prevented by a variable glucose infusion, neither epinephrine nor glucagon was able to counteract the suppressive effect of insulin on glucose output. These findings suggest that a fall in blood glucose per se may reverse insulin-induced inhibition of glucose production independent of a rise in counterregulatory hormones and that the insulin antagonist effect of counter-regulatory hormones is modulated, at least in part, by blood glucose concentration.
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PMID:Blood glucose regulates the effects of insulin and counterregulatory hormones on glucose production in vivo. 44 11

To evaluate the influence of the parasympathetic nervous system on human glucagon secretion, we have measured the plasma immunoreactive glucagon (IRG) levels after the administration of edrophonium, bethanechol chloride, and 2-deoxyglucose, and have compared the IRG responses to hypoglycemia in normal, atropinized, and vagotomized man. Edrophonium administered i.v. and bethanechol chloride administered s.c. did not affect IRG levels. Two-deoxy-glucose resulted in symptomatic neuroglucopenia with resultant vagal discharge, as evidenced by increased gastric acid secretion; but no changes in IRG concentrations were observed. The IRG response to insulin-induced hypoglycemia in normal subjects was not influenced by the administration of atropine. In seven subjects with a truncal vagotomy and no increased gastric acid secretion during insulin-induced hypoglycemia, the IRG increases were indistinguishable from those of control subjects in terms of timing, peak level obtained, or total glucagon response. We conclude that the cholinergic system is unlikely to play an important role in modulating glucagon secretion in man.
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PMID:Evaluation of the control of glucagon secretion by the parasympathetic nervous system in man. 44 96

The response of gastric inhibitory polypeptide (GIP) levels to oral glucose in 11 insulin-dependent diabetics was compared to that in 8 age- and sex-matched healthy controls to determine whether they would show the pattern of GIP hypersecretion reported by other workers in maturity-onset, insulin-independent diabetes. One gram of glucose per kg bw resulted in a higher level of glycemia and a significantly diminished GIP response in diabetics when compared to controls (6,018 +/- 1,337 vs. 11,343 +/- 2,353 pg/ml.180 min min, respectively). There was virtually no beta cell response in the diabetics, as measured by changes in the levels of free insulin and connecting peptide. A significant lowering of glucagon levels occurred in the controls, while an inconsistent response was seen in the diabetics. An insulin infusion test was administered to test the hypothesis that insulin suppresses GIP secretion. Although hyperinsulinism, hypoglycemia, and suppression of endogenous insulin secretion were produced in the controls, no suppression of baseline GIP was detected. Similarly, hyperinsulinism and hypoglycemia failed to suppress baseline GIP levels in the diabetics. These results do not support a direct role for insulin in suppressing GIP in normal or diabetic subjects.
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PMID:Gastric inhibitory polypeptide response to hyper- and hypoglycemia in insulin-dependent diabetics. 45 45

The effects of acetylsalicylic acid (ASA), a known inhibitor of prostaglandin (PG) synthesis, on plasma glucose, insulin, glucagon and growth hormone (GH) responses to tolbutamide were examined in ten normal volunteers. Treatment with 3.2 g ASA daily for 3 days caused a significant reduction in basal plasma glucose levels (p less than 0.05); by contrast, basal insulin rose from 23 +/- 2 to 31 +/- 2 microU/ml (p less than 0.01). No significant changes in the basal concentrations of glucagon and GH were found after ASA. Insulin response to tolbutamide was significantly augmented after ASA (p less than 0.01) while GH response to hypoglycemia was reduced (p less than 0.05). The pattern of plasma glucose and glucagon was not significantly modified by the treatment. Since ASA seems to have an action opposite to PGE on insulin and GH secretion, it is possible that the ASA may work through inhibition of PG synthesis.
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PMID:Influence of acetylsalicylic acid on plasma glucose, insulin, glucagon, and growth hormone levels following tolbutamide stimulation in man. 48 Dec 13

The blood glucagon concentration (fasting and in insulin hypoglycemia) was determined by radioimmunoassay in diabetic patients, relatives of diabetic patients with a normal glucose tolerance test, patients with obesity and a group of normal weight subjects. The index of glucagon rise above the fasting level and glucagon release rate were estimated. In relatives of diabetic and obese patients the initial blood glucagon concentration did not differ from that of healthy subjects. However, during insulin hypoglycemia, glucagon secretion was significantly reduced, and in relatives of diabetic patients it also proved to be delayed. A comparison of glucagon and somatostatin changes in the above mentioned patients allows to suggest participation of the somatostatin mechanism in disorders of glucagon secretion.
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PMID:Glucagon secretion in subjects with prediabetes, diabetes mellitus and obesity. 50 63


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