Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The response of insulinoma tissue to glucose, alpha-ketoisocaproate, and the modifiers of insulin release, tolbutamide, isoproterenol, and acetylcholine, was studied. Tumor tissue was transplanted under the kidney capsule of 14 rats, and the tumor-bearing kidneys were perfused in vitro about 8 weeks later. The plasma glucose concentration of these animals was 85.0 +/- 7.0 mg/dl, while the plasma insulin concentration was 13.8 +/- 1.5 ng/ml (normal, 180.5 +/- 7.0 mg/dl and 2.6 +/- 0.5 ng/ml, respectively; n = 26). Glucose (30 mM) evoked a 3- to 5-fold increase in insulin secretion, similar to the increase seen when either 100 micrograms/ml tolbutamide or 0.5 micrograms/ml isoproterenol were added to the perfusion medium containing 5 mM glucose. Propranolol at 50 micrograms/ml, but not at 20 micrograms/ml, inhibited insulin release stimulated by isoproterenol. Acetylcholine (10 or 100 microM) did not stimulate insulin secretion. alpha-Ketoisocaproate caused the highest insulin release of all stimuli studied. Glucagon or somatostatin release was not seen in any of the experiments. These results show that the tumor tissue transplanted under the kidney capsule responds not only to model fuels, but also to the sulfonylurea class of drugs and to adrenergic agents.
 ...
PMID:Pharmacological modifications of insulin release in vitro from fuel-responsive transplantable insulinomas. 614 33

Catheterization of the portal vein and stereotaxic implantation of electrodes in the lateral hypothalamic area (LHA) were performed in normal rats after thiopental anesthesia. Immunoreactive glucagon (IRG) and insulin (IRI), glucose, catecholamines, and beta-endorphin were monitored in portal and peripheral plasma, before and during electrical stimulation of the LHA. The influences on glucose and hormone concentrations of propranolol, phentolamine, atropine, and naloxone infusions were also investigated in similar rats. A basal portoperipheral concentration gradient was found for IRG, IRI, and catecholamines, but not for beta-endorphin. The LHA stimulation induced a significant rise in portal catecholamine, IRG, and glucose concentrations; IRI remained unchanged; the portoperipheral catecholamine gradient was augmented. These alterations were not observed after bilateral splanchnicectomy. Propranolol infusion abolished the LHA-dependent IRG and glucose rises. Naloxone reduced the IRG rise significantly. Phentolamine and atropine did not modify the LHA-induced reactions. These results suggest that the glucagon release which follows LHA electrical stimulation depends mainly on beta-adrenergic transmission by the splanchnic nerves. Opioid peptide receptors may modulate this effect.
 ...
PMID:Glucagon release after stimulation of the lateral hypothalamic area in rats: predominant beta-adrenergic transmission and involvement of endorphin pathways. 630 29

Previous studies have shown that sympathetic factors and blood glucose are of importance in the development of seizures and lung damage from OHP. In the present study we examined the influence of beta sympathetic agonists and blocking agents and glucagon on OHP toxicity. Rats were exposed to 6 ATA OHP and examined for time-to-seizure and lung damage. Pretreatment with propranolol increased the time-to-seizure by 70% and practolol by 50% without altering gross lung appearance or lung wet wt/dry wt. Propranolol and practolol also prevented brain glycogen depletion prior to seizure which otherwise occurred in subconvulsive exposure to OHP. Isoproterenol and glucagon pretreatment had no effect on time-to-seizure but isoproterenol did increase lung injury. Both practolol and propranolol block the beta-receptor influence on adenyl cyclase-stimulated second messenger production, while both isoproterenol and glucagon activate adenyl cyclase to produce second messenger. Our results may suggest a possible role for second messenger in mediating some of the acute toxic effects of OHP on the CNS.
 ...
PMID:Beta adrenergic receptors and glucagon in seizures from exposure to oxygen at high pressure (OHP). 631 53

Hypoglycemia is frequently reported in hemodialysis patients on propranolol. We studied the influence of propranolol on carbohydrate metabolism in sixteen hemodialysis patients (eight on propranolol and eight not) with pre-dialysis oral glucose tolerance tests (OGTT) and pre- and post-dialysis glucagon tests. Propranolol was shown to have significant suppressive effect on the insulin response during OGTT. With glucagon challenge pre- and post-dialysis, despite a similar cAMP response, patients on propranolol had significantly lower glucose response than those not receiving propranolol and it is postulated that this is due to post-receptor post-cAMP inhibition of hepatic glycogenolysis. Moreover, while the glucose response in patients not on propranolol significantly increased after dialysis, no significant change was found in patients on propranolol. The significantly higher C-peptide, insulin and cAMP responses to glucagon challenge in the hemodialysis patients as compared to normal controls may be due to delayed clearance of glucagon, and the further increased responses after dialysis may be due to the removal of a dialyzable factor suppressing these responses.
 ...
PMID:Effects of propranolol and hemodialysis on the response of glucose, insulin, C-peptide and cyclic AMP to glucagon challenge. 632 69

Two beta-blocking agents, non-selective propranolol and beta 1-selective metoprolol, were investigated with respect to their effect on glucose metabolism in 11 hypertensive, non-diabetic patients. They were randomly treated for two weeks in a double-blind cross-over manner with propranolol, metoprolol and placebo. Both drugs caused a small but significant increase in basal blood glucose values as compared with placebo (p less than 0.01). Metoprolol increased the blood glucose concentrations during the first 10 min of an i.v. glucose tolerance test (IVGTT) as compared with placebo (p less than 0.02) and propranolol (p less than 0.05). Propranolol raised only the blood glucose values during the later part of the IVGTT (p less than 0.01). The increase in blood glucose concentrations was, however, not associated with significant changes in peripheral insulin levels. The mean basal glucagon concentrations were lower during propranolol and metoprolol than during placebo (p less than 0.01). Propranolol also induced a more pronounced reduction of plasma glucagon than placebo (p less than 0.05) at 10 min of the IVGTT. The mean basal free fatty acid (FFA) concentrations were lower during propranolol (p less than 0.001) and metoprolol (p less than 0.05) than during placebo. Both drugs decreased the plasma levels of FFA during the first 10 min of the IVGTT as compared with placebo (p less than 0.01 and p less than 0.02, respectively). Pharmacological doses of propranolol and metoprolol increased blood glucose concentrations, decreased plasma glucagon and FFA concentrations, but had no effect on serum insulin levels in hypertensive, non-diabetic subjects.
 ...
PMID:Influence of beta-blocking drugs on glucose metabolism in hypertensive, non-diabetic patients. 633 83

The effects of nonselective beta-blockade (propranolol) and beta-1-selective blockade (atenolol) on glucose metabolism during insulin-induced hypoglycemia were studied in eight normal subjects during constant infusion of 3-[3H]glucose. Propranolol and to a lesser extent atenolol prolonged the hypoglycemic response to insulin. After maximal hypoglycemia a significant increase in glucose uptake rate was seen after propranolol and a corresponding trend was found in the atenolol experiments. The two beta-blockers did not influence glucose production rate after insulin administration. FFA concentration declined rapidly after insulin. Propranolol delayed the subsequent normalization of FFA whereas atenolol had no significant effect. Propranolol increased epinephrine and GH responses to hypoglycemia, whereas atenolol had no effect. Neither of the two beta-blockers influenced the concentrations of glucagon, norepinephrine, and PRL. It is concluded that nonselective beta-blockade prolongs the hypoglycemic response to insulin through an increased tissue uptake of glucose which is not counteracted by an increased glucose production. It is suggested that nonselective beta-blockade increases muscle glucose uptake by lowering FFA concentrations. beta-Blocker inhibition of the antiinsulin effect of epinephrine on glucose uptake in muscle can, however, not be excluded.
 ...
PMID:Effects of nonselective and beta-1-selective blockade on glucose metabolism and hormone responses during insulin-induced hypoglycemia in normal man. 633 40

Islet-activating protein (IAP) is a substance purified from the culture medium of Bordetella pertussis, and its main action is characterized by the enhancement of secretory response to glucose and other stimuli in pancreatic islet. In this experiment, the effect of IAP on epinephrine-induced secretion of immunoreactive insulin (IRI) and glucagon (IRG) was investigated in normal dogs. Epinephrine suppressed IRI secretion and it had a little increment to IRG secretion in control group, while IRI and IRG secretions were significantly increased by epinephrine in IAP pretreated group. Using beta-blocker (Propranolol) with epinephrine, these increments of IRI and IRG secretions in IAP pretreated group were abolished. However, using alpha-blocker (Phentolamine) with epinephrine, these secretions of IRI and IRG in IAP pretreated group were much more increased than epinephrine alone induced secretions. Blood glucose levels were lower in IAP pretreated group than in control group throughout the loading tests in all of the experiments. These findings suggest that (1) IAP decreases blood glucose level and (2) IAP enhances epinephrine-induced secretion of insulin and glucagon by acceleration of beta-adrenergic effect and by reduction of alpha-adrenergic suppression in dogs.
 ...
PMID:Islet-activating protein (IAP)-induced adrenergic modulation of pancreatic A and B cell in dogs. 637 Aug 19

In order to evaluate the influence of beta-adrenergic blockade on recovery from insulin-induced hypoglycemia, we compared the effect of saline or propranolol infusion during concomitant hypoglycemia in normal and type I diabetic persons. The diabetic subjects were initially rendered euglycemic with a basal insulin infusion. Glucose turnover was measured using [3-3H]glucose tracer. Propranolol caused a small but significant delay in glucose recovery in normal subjects, with plasma glucose only 80% of the values seen during saline infusion 1 h after hypoglycemia (P less than 0.005). This delay was caused by a 70% reduction in the rebound glucose output, which was responsible for posthypoglycemic recovery. In the diabetic subjects, glucose recovery was significantly delayed as compared with that in normal persons, even in the absence of propranolol, and associated with reduced secretion of epinephrine and glucagon. Moreover, the addition of propranolol caused a further 50% reduction in glucose recovery such that plasma glucose remained below 50 mg/dl for 3 h. In contrast to normals, propranolol did not inhibit the already blunted rebound in glucose output. However, propranolol prevented the decline in glucose utilization that occurred when saline alone was infused. During saline infusion, glucose uptake was at basal rates by 60 min whereas, during propranolol administration, glucose uptake remained above baseline until 180 min (P less than 0.01). Thus, propranolol may interfere with glucose recovery after insulin-induced hypoglycemia in diabetic patients by blocking epinephrine's inhibition of glucose utilization whereas, in normals, propranolol's effect is largely accounted for by blockade of epinephrine-induced hepatic glucose production.
 ...
PMID:Effect of propranolol on delayed glucose recovery after insulin-induced hypoglycemia in normal and diabetic subjects. 637 11

The serum of hypothermic animals shows in vitro the ability of mobilizing fatty acids from the adipose tissue. This ability is quantitatively comparable to the lipolytic activity of glucagon but is lower than that of adrenaline. Propranolol decreases the lipid-mobilizing activity in the serum of hypothermic animals in vitro. Similarly insulin added to the medium with the serum of hypothermic animals decreased the lipid-mobilizing activity.
 ...
PMID:Effect of certain factors modifying the lipid-mobilizing activity in vitro in the serum of rats during hypothermia. 638 43

Norepinephrine, dopamine and serotonin directly stimulated glucagon secretion by isolated perifused hamster islet. Propranolol blocked norepinephrine, dopamine and serotonin-stimulated glucagon release, suggesting that norepinephrine, dopamine and serotonin may modulate glucagon secretion via a beta-adrenergic mechanism. Dopamine and serotonin may exert their action directly via the beta receptor, stimulate residual adrenergic nerve terminals, or the release of other islet biogenic amines. We conclude that part of the stimulating effect of norepinephrine on glucagon release is beta adrenergically mediated and that dopamine and serotonin may affect glucagon secretion either directly or through the release of neurotransmitters that lead to glucagon release. Thus the intra-islet released dopamine and serotonin may contribute to the islets paracrine system by stimulating intra-islet adrenergic neurons.
 ...
PMID:Biogenic amine regulation of glucagon secretion. 639 23


<< Previous 1 2 3 4 5 6 7 8 Next >>