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)

Patients with type 1 diabetes mellitus (IDDM) show augmented GH secretion, which is implicated in the pathogenesis of microvascular complications. On the other hand, it is well known that beta-adrenergic receptors have inhibitory influence on GH secretion, likely via stimulation of hypothalamic somatostatin. Since the possibility of pharmacological suppression of GH secretion would be of value in IDDM, we investigated the effect of salbutamol (SAL, 4 mg orally at -60 min) on the GH response to GHRH (1 micrograms/kg iv at 0 min) in 6 well-controlled (mean HbA1c +/- SEM: 7.3 +/- 0.5%) patients with IDDM. Salbutamol was able to inhibit basal GH levels (p < 0.05) as well as to abolish the GHRH-induced GH rise. After SAL administration, a significant (p < 0.05) reduction of glucagon levels was also found. Our data show that the enhancement of beta 2 adrenergic activity by oral therapeutical doses of SAL inhibits basal and GHRH-stimulated GH secretion in patients with IDDM.
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PMID:Inhibition by salbutamol of GHRH-induced GH release in type 1 diabetes mellitus. 133 41

Twenty-five patients with acute severe asthma were treated with oxygen, corticosteroids and either salbutamol or aminophylline by intravenous infusion. Blood glucose, plasma insulin and glucagon were measured during the first 24 hours of treatment. Salbutamol and aminophylline rapidly caused hyperglycaemia, accompanied by a rise in insulin and a fall in plasma glucagon. At first the increase in plasma insulin was insufficient to restore normoglycaemia, but by 24 hours homeostasis was restored. The early submaximal insulin response was attributed to the fasting caused by breathlessness. There was no evidence of an increase in hormone secretion caused by direct beta 2-adrenergic stimulation of the pancreatic islets. The effect of corticosteroids on blood glucose over the period of study was considerably less than the contribution of either salbutamol, or aminophylline.
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PMID:Mechanisms of abnormal glucose metabolism during the treatment of acute severe asthma. 143 70

Salbutamol-induced diabetic ketoacidosis having recently been reported, the authors have studied the metabolic changes produced by the drug in 6 nondiabetic patients. All patients received a 3-hour infusion of salbutamol (S) 20 z g/minm. On the following day, three of these were given somatostatin (SRIF) 100 mg/hour mixed with S infused at the same rate, whilst the remaining 3 patients received SRIF alone. On the 3rd day, patients of the first sub-group received the same infection of S and SRIF as before plus exogenous glucagon 90 ng/kg/hour. Somatostatin is know to inhibit insulin and glucagon secretion. Exogenous glucagon was given in order to reproduce the metabolic conditions of insulin-deficient diabetes mellitus. Salbutamol alone induced a small rise in blood glucose and insulin, free fatty acids, glycerol and ketonic bodies, but no changes in endogenous glucagon. SRIF alone produced no significant metabolic variations. In the presence of SRIF, all salbutamol-induced metabolic changes were increased. Adding glucagon mainly resulted in high levels of ketonic bodies. All variations correlated with each other. Thus, whilst the hyperglycaemic, lipolytic and ketogenic effects of S in non-diabetic patients are partly masked by insulin hypersecretion, they are enhanced in the absence of insulin and, to an even greater extent, by an excess of glucagon. Diabetic patients treated with salbutamol should therefore be under close surveillance and have their insulin dosage increased.
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PMID:[Metabolic risks of salbutamol in diabetic patients. A study using somatostatin (author's transl)]. 610 23

Because many communities lack prehospital advanced life support (ALS) services, increasing public access to such care is important. The present study was completed to establish an epidemiological database defining prehospital pharmacotherapeutic interventions by ALS rescue teams, in the hope of developing recommendations for medication administration by non-ALS personnel. Data were collected on 333 patients, including indication for pharmacotherapy, patient age, ambulance field time, route of medication administration, adverse effects of pharmacotherapy, efficacy of pharmacotherapy, additional ALS interventions, and patient medication/past medical history. Medications studied included albuterol nebulizer treatments (albuterol), aminophylline, amyl nitrite, atropine, bretylium tosylate, dexamethasone sodium phosphate, dextrose 50% (D-50), diazepam, diphenhydramine, dopamine, epinephrine 1 mg/1 mL, epinephrine 1 mg/10 mL, furosemide, glucagon, ipecac, isoproterenol, lidocaine, morphine sulfate, naloxone, nitroglycerin tablets (nitroglycerin), sodium bicarbonate, and verapamil. Albuterol, D-50, and nitroglycerin were used more often than other medications, accounting for total pharmacotherapeutic interventions for 228 persons (68.47% of total patients), including 100% of all pediatric patients. Partial pharmacological needs for an additional 20 patients also were satisfied by these agents. In all, albuterol, D-50, and nitroglycerin accounted for 250 of 395 total medication interventions (63.29%). No inappropriate use, point estimate [(0)/(333) (0.00% to 0.90%)], or unmet need, point estimate [(0)/(3,613) (0.00% to 0.08%)], of care was noted. When faced with communities lacking ALS rescue services, albuterol, D-50, and nitroglycerin are recommended for administration by emergency medical technician-ambulance and intermediate level rescuers, because of the high rate of use, relative ease of administration, and high benefit/low complication rates associated with these medications.
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PMID:Prehospital pharmacotherapeutic interventions: recommendations for medication administration by EMT-A and EMT-I personnel. 794 2