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)

Defibrillation after prolonged ventricular fibrillation (VF) is frequently followed by asystole or electromechanical dissociation (EMD) which are usually fatal. We studied the effects of glucagon, a known inotropic and chronotropic agent, during 19 episodes of postcountershock asystole/EMD in nine dogs. Systolic and diastolic aortic (Ao), left ventricular, pulmonary arterial, and right atrial (RA) pressures were recorded as was the instantaneous Ao-RA difference (coronary perfusion pressure) and coronary sinus blood flow (CSF) during closed-chest CPR. VF was induced electrically; 2 min later, a 400-J transthoracic shock was given. Countershock was always followed by asystole (n = 12) or EMD (n = 7). Conventional closed-chest CPR with a mechanical device was begun 30 to 60 sec after countershock and continued for 2 to 3 min. If a perfusing rhythm did not occur, glucagon (1 mg) was given iv and CPR continued for 2 to 3 min more. Glucagon had no significant effect on intravascular pressures, the coronary perfusion gradient, or CSF when compared to CPR alone. However, in 14 or 19 postcountershock episodes unresponsive to CPR alone, glucagon restored effective spontaneous circulation, i.e., successful cardiac resuscitation, due to its effects on the intrinsic pacemaker discharge rate. Glucagon has been previously shown to stimulate myocardial adenyl cyclase via nonadrenergic mechanisms. We conclude that when postcountershock asystole/EMD occurs, glucagon has a direct and favorable effect on cardiac resuscitation outcome due to its effects on pacemaker discharge rate which is not mediated by changes in myocardial blood flow or coronary perfusion pressure.
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PMID:Postcountershock pulseless rhythms: hemodynamic effects of glucagon in a canine model. 356 24

Reported is the case of a 17-year-old woman who experienced full cardiac arrest less than one hour after ingesting 8 g of propranolol. More than two hours of CPR were required because she did not respond to glucagon or high doses of beta and alpha agonists. An intra-aortic balloon pump was used for hemodynamic support of drug-induced cardiogenic shock when pulses returned. She experienced complete recovery without sequelae.
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PMID:Massive propranolol overdose poorly responsive to pharmacologic therapy: use of the intra-aortic balloon pump. 368 4

Since the C-peptide Radioimmuno active/Immuno Reactive Insulin (CPR/IRI) molar ratio is considered as an index of insulin hepatic extraction and tissue receptor binding, the AA. investigated the effects of metformin on this index after glucagon infusion in non-insulin dependent diabetics. Fourteen lean subjects (aged 48 to 67 years, mean 54 +/- 7) with non-insulin dependent diabetes were studied. At 9.00 a.m. each subject after overnight fasting, underwent glucagon infusion (1 mg i.v. diluted in 250 ml of saline, infused at a rate of 8.3 gamma/min for 2 hours); blood specimen were obtained at --15, 0, 30, 60, 90, 120 min. This test was repeated after a five-day treatment with metformin (1.5 g per os). For each sample plasma glucose by glucose oxidase method, plasma insulin and C-peptide by Radio Immuno Assay (RIA) method were determined. After treatment with metformin the hyperglycemia induced by glucagon was not influenced; nevertheless insulin and C-peptide plasma levels showed an evident reduction while CPR/IRI molar ratio was unchanged. The AA. suppose an indirect effect of metformin upon beta cells, namely a less pancreatic insulin requirement, mediated by an improvement of glucose utilization.
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PMID:Effect of metformin on blood glucose, insulin and C-peptide responses to glucagon in non-insulin dependent diabetics. 634 93

Hepatic and pancreatic damage owing to iron overload is often present in patients with beta-thalassemia major. In order to investigate B-cell function and hepatic insulin clearance in these patients, under a high transfusion program and regular chelation therapy, we studied the glucose (BG), insulin (IRI) and C-peptide (CPR) response and the CPR/IRI ratio after OGTT in 27 patients with Cooley's anemia and in 10 sex- age- and weight-matched healthy subjects; we also studied BG and IRI levels after IVGTT in 9 beta-thalassemic patients and in 9 control subjects. Furthermore, BG, CPR, IRI and glucagon (IRG) response to arginine infusion were evaluated in 5 thalassemic patients with normal OGTT and in 5 age-, sex- and weight-matched normal children, in order to assess pancreatic A-cell function, too. OGTT and IVGTT were normal in the patients with beta-thalassemia major. Plasma IRI level 30 min after an oral glucose load and the insulinogenic index for cumulative intervals were significantly lower in thalassemics after OGTT, whereas the insulin response and insulinogenic index were normal following i.v. glucose. No significant difference was observed for the CPR/IRI ratio during OGTT between thalassemics and normal subjects. Finally, BG, CPR, IRI and IRG levels were similar in the thalassemic patients and in healthy children both fasting and following arginine infusion. Our data suggest that patients with beta-thalassemia major, under a high transfusion program and regular chelation therapy, may have normal glucose tolerance and normal hepatic insulin clearance in spite of iron overload in pancreas and liver. Insulin response to oral glucose was lower than the one to IVGTT, probably because of diminished secretion of the gastrointestinal hormones which stimulate insulin release.
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PMID:Study of A- and B-cell function in beta-thalassemia major. 634 2

To determine how total pancreatectomy influences the secretion of gut glucagon in man, 15 totally pancreatectomized patients (Px), 14 distally gastrectomized patients (Gx), and 15 healthy subjects were investigated by intravenous arginine infusion test and oral glucose tolerance test. Blood glucose, plasma insulin (IRI), and C-peptide (CPR) levels were determined. Plasma immunoreactive glucagon (IRG) and total glucagon-like immunoreactivity (total GLI) were also measured. Gut glucagon-like immunoreactivity (gut GLI) was calculated to be the difference between total GLI and IRG. In the Px group, arginine infusion did not significantly alter the levels of IRI, CPR, IRG, and gut GLI. Mean basal value of gut GLI in the Px group of 356 +/- 40 pg/ml was significantly higher than 179 +/- 26 pg/ml of the healthy (p less than 0.01) and 182 +/- 24 pg/ml of Gx group (p less than 0.01). Oral glucose loading led to the highest increase of gut GLI in the Px group (p less than 0.01). Thus, extrapancreatic IRG may not be secreted into the plasma in totally pancreatectomized humans in response to arginine stimulation. Complete absence of the pancreas and the deficiency of insulin-effect may lead to a hypersecretion of gut GLI, both in the basal state and after oral glucose loading.
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PMID:Effects of total pancreatectomy on the secretion of gut glucagon in humans. 635 Jun 63

Plasma level of immunoreactive insulin (IRI) and C-peptide (CPR), and their responses to intravenous administration of glucagon were studied in 37 patients with cirrhotic portal hypertension during hepatic vein catheterization. IRI and CPR in peripheral vein and hepatic vein were compared with development of portal vein collaterals measured by indocyanine green disappearance tests and portal venograms. In additional 2 cases, the values were compared with those of portal vein blood obtained by percutaneous transhepatic catheterization. Plasma IRI of peripheral vein in cirrhotic patients, those who had only esophageal varices but did not have remarkable amount of portal vein collateral blood flow, revealed the changes closely resembling the controls. On the contrary, peripheral vein IRI elevated significantly in cirrhotics with large shunt and the values exceeded those of hepatic vein, although responses to the glucagon test were normal. In experimental study using dogs, peripheral IRI revealed significant increase after the portocaval anastomosis diverting the portal blood containing high IRI into the inferior vena cava, and the values exceeded those of hepatic vein. It is important to know the development of portal vein collaterals as a major cause of hyperinsulinemia in liver cirrhosis.
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PMID:[Clinical and experimental studies on elevated plasma level of insulin in cirrhotic patients with portal hypertension and portosystemic collateral circulation]. 637 13

In order to clarify the mechanism of insulin secretion, responses of insulin (IRI) and C-peptide (CPR) in plasma to various stimuli were investigated in normal subjects and patients with diabetes mellitus, liver cirrhosis, chronic nephritis or insulinoma. The response of plasma IRI and CPR to oral glucose load was less marked in the mild and moderate diabetes groups than in the normal controls. Neither IRI nor CPR in the severe diabetes group responded to oral glucose. The patients with liver cirrhosis revealed an exaggerated and delayed response of IRI and CPR, and a lowered CPR/IRI ratio, indicating a remarkable response of IRI to glucose. In contrast, the patients with chronic nephritis showed a prominent rise of CPR alone. In the insulinoma patients, both plasma IRI and CPR increased after glucose load. In the response to glucose, there was approximately 30-min lag time between the peaks of IRI and CPR in the normal controls and the patients with various diseases. Following arginine infusion, plasma IRI and CPR increased in the normal subjects and the patients with moderate diabetes. In the normal subjects, plasma IRI reached a peak at 6 min and 3 min in response to tolbutamide and glucagon, respectively, which elicit an abrupt and sharp rise of insulin from B-cells. However, diabetic patients showed a minimal change in plasma IRI and CPR, whereas there was an exaggerated response of plasma IRI and CPR in insulinoma patients. In analysis of responses of plasma IRI and CPR to tolbutamide or glucagon, there was a lag time longer than 10 min in the normal subjects. The present study confirms the concurrent release of C-peptide from the B-cells in the secretion of insulin. In addition, it was suggested that insulin and C-peptide are mainly handled in the liver and the kidney, respectively. Furthermore, a longer lag time between the peaks of IRI and CPR in response to tolbutamide or glucagon did not necessarily indicate a simultaneous release of insulin and C-peptide from the B-cell, but a delayed release of the latter.
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PMID:Analysis of insulin secretion based on changes in plasma insulin and C-peptide in man. 676 99

Hormonal and metabolic characteristics of diabetes mellitus in the elderly were investigated in the following groups; elderly DM subdivided into obese DM and non-obese DM, elderly non-DM subdivided into obese and non-DM and non-obese non-DM, adult DM and adult non-DM. Responses of plasma glucose, insulin and glucagon during oral glucose tolerance test (OGTT), arginine tolerance test (ATT) and intravenous glucose tolerance test (IVGTT) were measured individually and the daily urinary C-peptide excretion (U-CRP), fasting plasma levels of free fatty acid (FFA), triglyceride (TD), total cholesterol (TC) and HDL-cholesterol (HDL-C) were also measured. In comparison with adults, insulin responses in IVGTT and ATT in elderly non-DM were low but not in OGTT. It was noteworthy that glucagon response during OGTT in elderly DM was considerably lower than adult DM, probably due to factors other than insulin deficiency. Comparing elderly DM and elderly non-DM, the initial response of insulin in OGTT was found to be low in elderly DM but not in total response. In the comparison between the obese and the non-obese, higher insulin levels in elderly obese DM than in elderly non-obese DM during OGTT, IVGTT and ATT were observed, implying decreased insulin sensitivity. This difference, however, was not apparent between elderly obese non-DM and non-obese non-DM. A good correlation between U-CPR and the response of plasma insulin in OGTT was shown even in the elderly but not between U-CPR and that of plasma insulin in IVGTT.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hormonal and metabolic aspects of diabetes mellitus in the elderly]. 831 43

Elevated plasma levels of plasminogen activator inhibitor-1 (PAI-1) have been shown to be a risk factor for the development of vascular complications in obese and hyperinsulinemic non-insulin-dependent diabetes (NIDDM) patients. To clarify whether PAI-1 also plays an essential role in the development of such complications in NIDDM patients without obesity or hyperinsulinemia, PAI-1 was analyzed in relation to blood pressure, fasting plasma levels of glucose (FPG), hemoglobin A1C (HbA1c), immunoreactive insulin (F-IRI), C-peptide (CPR), total cholesterol (TC), triglyceride (TGL), and HDL-cholesterol (HDL-C) in 77 NIDDM patients and 10 healthy control subjects. The NIDDM patients were not obese (body mass index [BMI]:<26 kg/m2) or hyperinsulinemic, and BMI in the controls was between 19 and 24 kg/m2. In addition, parameters of insulin secretion reserve, including sigmaIRI, insulinogenic index, and CPR at 5 min after glucagon loading, were evaluated simultaneously. Plasma levels of PAI-1 were higher in the NIDDM group (9.3+/-0.9 ng/ml) than in the controls (4.3+/-0.7 ng/ml;P<0.01). Levels of FPG and HbA1c were also elevated in the NIDDM group (P<0.05 for each), but F-IRI did not differ between the two groups. However, multiple regression analysis revealed no significant correlation in the NIDDM between PAI-1 and F-IRI or the parameters of insulin secretion reserve. Regardless of the presence or absence of vascular complications, PAI-1 did not vary significantly in the NIDDM. These findings suggest that the effects of PAI-1 on the development of diabetic complications in NIDDM patients may not proceed in the same way in those with versus those without obesity or hyperinsulinemia, because no correlation was found between PAI-1 and insulin secretion reserve, while plasma levels of PAI-1 were higher in the NIDDM group than in the controls.
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PMID:Plasminogen activator inhibitor-1 in nonobese subjects with non-insulin-dependent diabetes mellitus. 863 10

In order to evaluate the steady state plasma glucose (SSPG) method by using a new somatostatin derivative, octreotide acetate (Sandostatin) instead of somatostatin that we had used for the insulin sensitivity test, we examined whether octreotide was able to suppress C-peptide (CPR), glucagon (IRG), and GH to a similar degree to that achieved with somatostatin. A total of 52 studies were performed in 45 essential hypertensive subjects and 7 healthy subjects. Octreotide was given subcutaneously in a does of 50 micrograms or 100 micrograms 10 min before the test (sc 50, sc 100 groups) or intravenously infused over 2 h (10 micrograms in bolus followed by a constant infusion, 50, 100, or 150 micrograms/2 h: i.v. 50, i.v. 100, i.v. 150 groups). In all of the groups the plasma immunoreactive insulin (IRI) concentration increased gradually after insulin injection and reached the steady state plasma insulin (SSPI) level between 40 and 60 microU/ml at 60 min through 120 min. Plasma CPR at 120 min was the most suppressed (by 67% of the basal level in i.v. 150 group during the study period), but on the other hand in both the sc 100 and i.v. 100 groups the plasma CPR concentration at 120 min was suppressed by nearly 40%, but not significantly suppressed in either the sc 50 or the i.v. 50 group. Plasma IRG and GH were strongly suppressed after 60 min in all groups during the study period. Plasma glucose had increased significantly at 30 min and reached the steady state at 90 min through 120 min in hypertensive and healthy subjects. The results indicated that the modified SSPG method with continuous intravenous infusion of Octreotide at 150 micrograms/2 h was adequate for the measurement of insulin sensitivity.
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PMID:Modified method using a somatostatin analogue, octreotide acetate (Sandostatin) to assess in vivo insulin sensitivity. 873 63


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