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)

The effect of intravenous application of 1 mg glucagon on serum magnesium concentration, potassium, immunoreactive insulin (IRI), and blood glucose in healthy subjects has been studied. A significant decrease of the serum magnesium concentration was observed beginning 5 min after glucagon injection. There is a tendency of a slight but not statistically significant decrease of potassium level at 60 min. The beginning of the decrease of magnesium level was associated with the maximum of IRI-peak. In contrast to the discussed hypothesis that hyperglycemia and hyperinsulinemia cause a shift for magnesium and potassium from the extracellular into the intracellular space we could demonstrate that hyperglycemia is not a necessary condition for the decreasing effect of glucagon on serum magnesium level.
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PMID:Investigations on changes of serum magnesium concentration after glucagon application in healthy humans. 73 15

A number of hemodynamic, pharmacologic, and metabolic interventions were found to change the extent of acute ischemic injury of the myocardium and subsequent necrosis following experimental coronary artery occlusion. Reduction in myocardial damage occurred by decreasing myocardial oxygen demands (beta-adrenergic blocking agents, intra-aortic balloon counterpulsation, nitroglycerin, decreasing afterload in hypertensive patients, inhibition of lipolysis, and digitalis in the failing heart); by increasing myocardial oxygen supply either directly (coronary artery reperfusion or elevating arterial pO2), or through collateral vessels (evevation of coronary perfusion pressure by alpha adrenergic agonists, intra-aortic balloon counterpulsation); or by increasing plasma osmolality (manitol, hypertonic glucose); presumably by augmenting anaerobi metabolism (glucose-insulin-potassium, hypertonic glucoxe insulin potassium, hypertonic glucose); by enhancing transport to the ischemic zone of substrates utilized in energy production (hyaluronidase); by protecting against autolytic and heterolytic damage (hydrocortisone, cobra venom factor, aprotinin). Augmentation of myocardial ischemic damage occurred as a consequence of increasing myocardial oxygen requirements (isoproterenol, glucagon, ouabain, bretylium tosylate, tachycardia); by decreasing myocardial oxygen supply either directly (hypoxia, anemia), through reduction of collateral flow (hemorrhagic hypotension, minoxidil), or by decreasing substrate availability (hypoglycemia). Pilot studies have been carried out in patients with hyaluronidase, nitroglycerin intra-aortic balloon counterpulsation, beta-blocking agents and Arfonad and have shown that these interventions may also reduce myocardial damage, which suggests that the concept of reduction in infarct size following coronary occlusion is applicable clinically.
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PMID:Effects of metabolic and pharmacologic interventions on myocardial infarct size following coronary occlusion. 76 15

Diabetes mellitus is more frequently found in pateints with hepatic cirrhosis (about 10%) than in subjects without liver disease. Cirrhosis has been the main subject of interest in this respect. Very few studies have been made in viral hepatitis or steatosis. In about 40% of cases, the diabetes is identified before the cirrhosis. More often (in about 60% of cases) the diabetes is discovered at the same time as or after the finding of cirrhosis. This "post-cirrhosis diabetes" shows no clinical peculiarity. In about 80% of patients with liver cirrhosis when fasting blood glucose is normal, abnormalities of carbohydrate metabolism are to be found by the oral glucose tolerance test. Approximately 50% show an abnormal response to intravenous glucose and 30% to intravenous tolbutamide. The "mechanism" of these metabolic abnormalities in liver cirrhosis is unknown. The following abnormalities are observed: 1) With similar glycaemic response to a glucose challenge, plasma insulin levels are higher than in patients without liver disease, suggesting insulin unresponsiveness. Resistance to exogenous insulin can be demonstrated. 2) Plasma free fatty acid levels are often elevated. 3) Plasma growth hormone levels are often raised. 4) Plasma glucagon levels are high when porto-caval shunting is present. 5) Potassium is often depleted. These metabolic abnormalities, in association with porto-caval shunting and hepatocyte insufficiency may explain the insulin resistance which characterises liver cirrhosis, and the diabetes which it may precipitate in predisposed persons.
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PMID:[Diabetes mellitus secondary to liver diseases. A review (author's transl)]. 79 27

Carbohydrate metabolism is temporarily disturbed in acute myocardial infarction. The degree of hyperglycaemia and failure of response of insulin appears to be related to the severity of the infarction. The underlying hormonal changes probably include increased secretion of catecholamines and of glucagon. Circulating free fatty acids (FFA) are generally increased by the same metabolic and hormonal factors which promote glucose intolerance. In the zone of developing infarction in the heart, there is a complex metabolic situation with glucose metabolism both being accelerated and inhibited by different factors. Continued uptake of FFA is associated with intracellular accumulation of activated long-chain FFA, acyl CoA, which tends to inhibit mitochondrial metabolism. The metabolism of glucose is thought to be beneficial and that of FFA detrimental to the infarcting tissue. Thus the glucose intolerance and the high circulating FFA occurring as part of the general metabolic response to myocardial infarction, are thought to be harmful to the ischaemic tissue. Increased provision of glucose by dichloroacetate, and inhibition of FFA metabolism by nicotinic acid analogues decrease the extent of experimental infaraction, while glucose--insulin--potassium and propranolol act both by increasing glucose uptake and decreasing that of FFA. Glucose intolerance is also common in peripheral vascular disease. The reasons for this are obscure. However, the alterations in circulating insulin concentration which accompany this intolerance may be involved in the development of arterial lesions either directly through an effect on arterial wall synthesis or indirectly through an effect on circulating lipid levels. Defects may also be found in arterial wall mucopolysaccharide or sorbitol metabolism. The role of sex hormones and catecholamines remains speculative. At present the most cogent view is that in peripheral vascular disease a multi-hormonal disorder exists which may be contributing to the development of arteriosclerosis.
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PMID:Carbohydrate metabolism in cardiovascular disease. 79 85

To evaluate the effect of physiologic hyperglucagonemia on nitrogen and glucose metabolism and on urinary electrolyte excretion, pancreatic glucagon was administered as a continuous 3-day infusion to three adult-onset non-insulin-dependent diabetics and two insulin-treated juvenile diabetics while on a constant dietary intake. The glucagon infusion resulted in increases in plasma glucagon which were 4-6 fold greater than control values. Despite prolonged hyperglucagonemia, urinary glucose excretion was unchanged. Similarly, urinary urea nitrogen and total nitrogen excretion were not altered by glucagon administration. Urinary sodium tended to rise, albeit not significantly (p less than .01), on the first infusion day, but later declined to control values despite increasing plasma glucagon concentrations. Urinary chloride, potassium, calcium, phosphorus excretion remained unchanged. We conclude that continuous physiologic increments in plasma glucagon do not enhance glycosuria or increase protein catabolism and ureagenesis in diabetes when insulin is available. The augmented protein catabolism and glucogenesis that accompany diabetic ketoacidosis cannot be explained primarily on the basis of hyperglucagonemia.
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PMID:Influence of physiologic hyperglucagonemia on urinary glucose, nitrogen, and electrolyte excretion in diabetes. 83 43

Other investigators have shown that infusion of glucagon causes the concentration of potassium, [K+], in the arterial plasma to increase rapidly, then to decrease to less than the beginning value. In studies on anesthetized dogs, we found that the magnitude of the initial, rapid rise of [K+] was increased by nephrectomy but not affected by pancreatectomy. The subsequent decline of [K+] and the persistent hypokalemia were not affected significantly by nephrectomy. Plasma [K+] decreased in the nephrectomized-pancreatectomized dogs, as it did in the nephrectomized and the control groups, but the effect was temporary, and [K+] began to increase again, even though the infusion of glucagon continued; after the infusion was ended, plasma [K+] became significantly higher than the beginning value. These data suggest that the hypokalemia caused by infusion of glucagon initally depends on extrarenal factors other than insulin, and, later, depends on insulin.
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PMID:The contribution of renal and extrarenal mechanisms to hypokalemia induced by glucagon. 84 85

Blood glucose and serum potassium (K+) concentrations were measured before, during, and 60 minutes after operation in two groups of 10 patients during nitrous oxide/halothane/d-tubocurarine anesthesia for major orthopedic surgery. In the control group, arterial blood pressure was maintained within normal range, while in the study group trimethaphan camsylate was administered as an intravenous infusion (average, 218 mg.) to maintain a systolic blood pressure of 60 to 65 torr. In the normotensive group, blood glucose rose significantly during operation and early postoperatively and serum K+ was essentially unchanged. In the hypotensive group, trimethaphan caused a striking modification of surgically induced hyperglycemia, together with a small significant decrease in serum K+ intraoperatively. The observed increase in blood glucose is part of the autonomic response to surgical stress. Hormonal factors (growth hormone, cortisol and glucagon) may conceivably be involved. The decrease in serum K+ is probably caused by decreased hepatic glycogenolysis and attenuation of the suppressive effect of catecholamines on insulin release, both effects being secondary to the ganglionic blocking property of trimethaphan. These results indicate that trimethaphan, in contrast to other ganglionic blocking drugs, does not cause hypoglycemia and suggest that serum K+ concentration should be monitored whenever these drugs are used.
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PMID:Changes in serum potassium and blood glucose concentrations after trimethaphan administration in man. 93 27

Two Holstein bull calves each were infused intravenously with 1 mg glucagon in .9% sodium chloride, and two were given saline alone; 1 wk later treatments were reversed. Glucagon increased concentrations of insulin and glucose but decreased potassium in blood plasma and moderately increased urinary magnesium and calcium losses. When only saline was used, there was no effect. A hypothesis relating elevated glucagon to grass tetany is proposed.
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PMID:Effect of glucagon infusion on plasma magnesium, glucose, and insulin in bull calves. 96 39

Endogeneous hyperglucagonemia is observed in experimental diabetes mellitus and semistarvation, conditions associated with an increased intestinal absorptive function. To examine whether glucagon might exert a similar adaptive response on intestinal digestive-absorptive function like experimental diabetes mellitus the effect of chronic glucagon administration on intestinal transport of 3-0-methyl-D-glucose, water, sodium, potassium, and D-glucose induced transmural potential difference (PD) was examined by an in vivo perfusion technique in rat small intestine. Chronic administration of glucagon (100 mug twice daily) for 5 days resulted in increased absorption of 3-0-methyl-D-glucose, water, sodium and potassium as well as in an increase of D-glucose induced PD. A similar, but more pronounced augmentation of D-glucose induced PD was observed in the jejunum of streptozotocin-diabetic rats. Disaccharidase (maltase, sucrase, trehalase, lactase) and alkaline phosphatase activities were not affected in intestinal mucosa of glucagon-treated rats compared to controls. It cannot be decided from these results whether hyperglucagonemia is responsible for the adaptive intestinal changes observed in experimental diabetes mellitus.
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PMID:Effect of chronic glucagon-administration on the digestive and absorptive function of rat small intestine in vivo. 98 1

Tumoral secretions and pathophysiology of diarrhea were studied in 1 patient with pancreatic cholera. High concentrations of vasoactive intestinal peptide were found in both systemic blood and tumoral extracts, together with increased plasma levels of calcitonin and protaglandins E and Falpha. Gastric inhibitory peptide and gastrointestinal and pancreatic hormones were absent from the tumor, except for small amounts of glucagon, and their blood levels were normal. Decreased basal but normal pentagastrin-stimulated gastric acid secretion, normal basal and secretin-stimulated pancreatic secretion, increased volume of gallbladder bile with high bicarbonate, and low bile salt concentrations were observed, but the electrolyte content and flow rate of fluid passing the duodenojejunal junction were within normal limits. Small intestine was found to be the origin of the water and electrolyte fasting losses. Jejunum was the site of bicarbonate secretion. Jejunal glucose and leucine-stimulated water and sodium transports were also strikingly decreased, whereas the absorption rates of the sugar and amino acid were normal. Colon reabsorbed high amounts of water and sodium but increased potassium losses. Biological effects of vasoactive intestinal peptide may explain most of the patient's upper digestive secretion abnormalities and small intestinal function impairments, whereas secondary aldosteronism might explain the modified colonic function.
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PMID:Pancreatic cholera. Sudies on tumoral secretions and pathophysiology of diarrhea. 109 88


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