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)

1. The relationship between urea synthesis, intracellular N-acetylglutamate and the capacity of rat-liver mitochondria to synthesize citrulline was investigated. 2. Treatment of rats with glucagon prior to killing results not only in an increased intramitochondrial ATP concentration and an increased capacity of the mitochondria to synthesize citrulline, but also in an increased concentration of intramitochondrial N-acetylglutamate. 3. Comparison of the rate of citrulline synthesis in mitochondria from glucagon-treated and from control rats, incubated under different conditions, shows that the increased N-acetylglutamate concentration after glucagon treatment is at least in part responsible for the observed increased capacity of the mitochondria to synthesize citrulline. 4. Ureogenic flux in isolated hepatocytes under different incubation conditions correlated with the intracellular concentration of N-acetylglutamate and with the capacity of the mitochondria to synthesize citrulline. 5. When isolated hepatocytes were incubated with NH3, ornithine, lactate and oleate, intracellular N-acetylglutamate increased about eightfold in the first 10 min; during this period the rate of urea synthesis increased considerably. 6. It is concluded that the concentration of intramitochondrial N-acetylglutamate plays an important role in the short-term control of flux through the urea cycle under different nutritional and hormonal conditions.
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PMID:The relationship between intramitochondrial N-acetylglutamate and activity of carbamoyl-phosphate synthetase (ammonia). The effect of glucagon. 624 85

The reaction of nitromalondialdehyde with the arginine residues of glucagon results in the conversion of the 2 arginine residues in the peptide to delta-(5-nitro-2-pyrimidyl)ornithine to form di[delta-(5-nitro-2-pyrimidyl)ornithine 17,18]glucagon (NP-glucagon). The modified peptide does not exhibit any loss in ability to activate adenylate cyclase of rat liver plasma membranes or to stimulate glycogenolysis in cortisone-primed rabbits relative to the native hormone despite this marked alteration in structure. The CD of dilute solutions of NP-glucagon is similar to that of the native hormone. In the absence of salt, the CD of NP-glucagon is independent of peptide concentration, but structures of higher helical content are observed in concentrated peptide solutions in the presence of 0.1 M NaCl and in methanol. The extent of helix formation under these conditions is greater than that given by glucagon. Results from viscosity and proton magnetic resonance spectra confirm and extend previous studies to indicate that this fully active derivative is in a compact folded conformation.
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PMID:Conformational and biological properties of di[delta-(5-nitro-2-pyrimidyl)ornithine 17,18]glucagon. Role of the arginine residues. 629 99

The case of a female patient with fasting hypoglycaemia before the development of Type 1 (insulin-dependent) diabetes mellitus is reported. She presented with primary hypothyroidism, partial hypopituitarism, adrenal insufficiency and glucagon deficiency. Thyroid microsomal and gastric parietal cell antibodies were detected as well as HLA-B8, whereas islet cell antibodies were not demonstrable, even 2 years after the onset of diabetes. Plasma chromatography revealed true pancreatic glucagon (IRG3500) close to undetectable in basal samples with a questionable increase from 3 to 18 pg/ml during insulin-induced hypoglycaemia. After an overnight fast, moderate hyperaminoacidaemia was found with elevations of alanine, glycine, serine, arginine and ornithine as seen in pancreatectomized patients. It is suggested that the deficient glucagon secretion in this patient might, at least in part, have been the cause of fasting hypoglycaemia and the failure of glucose recovery following insulin-induced hypoglycaemia. Possible, the A cell deficiency was part of the polyglandular failure syndrome in this patient.
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PMID:Glucagon deficiency associated with hypoglycaemia and the absence of islet cell antibodies in the polyglandular failure syndrome before the onset of insulin-dependent diabetes mellitus: a case report. 635 16

Duodenopancreatectomy induces a severe glucagon deficiency and elevated plasma concentrations of alanine, aspartate, glycine, proline, serine, arginine, citrulline, ornithine, phenylalanine and tyrosine. Restoring high physiological plasma glucagon in six such patients by infusing 0.3 mg/24 h of exogenous glucagon reduced significantly (P less than 0.01 or 0.001) the mentioned amino acids (except phenylalanine) and further asparagine, glutamine, methionine and threonine. In six normal subjects the same infusion reduced significantly (P less than 0.05 to 0.001) plasma alanine, asparagine, glutamate, glutamine, glycine, proline, serine, threonine, arginine, ornithine, lysine and tyrosine. However, the effect was significantly (P less than 0.01 or 0.001) less marked for alanine, glutamine, glycine, methionine, serine, threonine and arginine. This particular glucagon sensitivity of duodenopancreatectomized patients suggests that glucagon deficiency is the cause of their hyperaminacidaemia. By contrast, lipoprotein concentrations were virtually unaffected by either glucagon deficiency or its replacement. In the light of the marked hypoaminacidaemia in glucagonoma patients these results attribute to glucagon a major role as a regulator of protein metabolism.
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PMID:Amino acids and lipoproteins in plasma of duodenopancreatectomized patients: effects of glucagon in physiological amounts. 640 37

The role of glucocorticosteroid and thyroid hormone and of glucagon and insulin in the pre- and postnatal developmental formation of carbamoyl-phosphate synthase, ornithine transcarbamoylase, arginase, glutamate dehydrogenase, tyrosine aminotransferase, glucose-6-phosphatase, hexokinase and glucokinase activities in rat liver was investigated. Glucocorticosteroids and a low insulin/glucagon ratio always stimulate formation of carbamoyl-phosphate synthase, ornithine transcarbamoylase, arginase, glutamate dehydrogenase, tyrosine aminotransferase and glucose-6-phosphatase, while glucocorticosteroids and a high insulin/glucagon ratio stimulate formation of glucokinase. Thyroid hormone stimulates the formation of carbamoyl-phosphate synthase, arginase and tyrosine aminotransferase only before birth, whereas it stimulates the formation of glutamate dehydrogenase and glucose-6-phosphatase both before and after birth. Ornithine transcarbamoylase activity is depressed after thyroid-hormone treatment before and after birth. DNA content is always decreased by glucocorticosteroids and increased by thyroid hormone. The effect of these hormones on hexokinase is complex, probably due to different responses of the constitutive isozymes. With the exception of the effects of thyroid hormone on carbamoyl-phosphate synthase, arginase and tyrosine aminotransferase before birth, which may be indirect, the responses of enzyme activities and DNA content to treatment with glucocorticosteroid hormones, glucagon, insulin and thyroid hormone are qualitatively the same in fetuses, neonates, sucklings, weanlings and adults. Thus, the developmental profiles of the enzyme clusters reflect the changing levels of the relevant hormones. The enzymes that are stimulated by glucocorticosteroids and the insulin/glucagon ratio show increases in enzyme activity perinatally and around weaning, and relatively low activities in between, while those enzymes that are additionally stimulated by thyroid hormone differ in exhibiting relatively high activities between birth and weaning.
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PMID:Multihormonal control of enzyme clusters in rat liver ontogenesis. II. Role of glucocorticosteroid and thyroid hormone and of glucagon and insulin. 702 60

A total of 5,473 pharmacological provocative growth hormone release tests were carried out in 3,143 children. Mean age was 9 years 9 months (range 3-16 years) and mean bone age was 7 years 6 months (range 2-14 years). Tests were of 9 different types: 1) arginine (n = 625); 2) clonidine (n = 339); 3) insulin (n = 198); 4) ornithine (n = 162); 5) insulin + arginine (n = 203); 6) clonidine + betaxolol (n = 2,003); 7) L-dopa (n = 685); 8) glucagon = propranolol (n = 443); 9) glucagon + betaxolol (n = 815). All growth hormone determinations were performed using the same radioimmunoassay. Distribution of values obtained with each test was gausso-logarithmic. Mean peak levels with their 95% confidence limit were as follows: 1) 10.2 and 0.45; 2) 11.5 and 0.7; 3) 11.8 and 0.8; 4) 14.2 and 1.2; 5) 14.3 and 0.9; 6) 15.7 and 1.1; 7) 19.8 and 2.1; 8) 20.8 and 2.3; 9) 21.0 and 2.5. These data indicate low specificity, with up to two-fold differences in mean peak levels from one test to another; proportions of peaks under 10 ng/ml ranged from 29% to 69%. Thus, the rate of patients diagnosed with growth hormone deficiency may vary substantially according to the test used. To reduce these discrepancies, we suggest adjustment of test results using a weighting coefficient of 1) 1.9; 2) 1.48; 3) 1.4; 4) 1.16; 5) 1.06; 6) 1.01; 7) 0.73; 8) 0.69; 9) 0.66.
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PMID:[Statistic study of 5,473 somatotropin secretion stimulation pharmacologic tests (n=9). Proposed weighting coefficient]. 823 89

Levels of plasma amino acids, ammonia, glucagon and insulin and their 5-hr responses to a protein feeding were evaluated before and sequentially (3 mo and 1 yr) after distal splenorenal shunt in 10 patients with cirrhosis belonging to Child-Pugh's class A or B. An index of glucagon effectiveness (plasma glucose/glucagon) was also calculated. These parameters were related to liver test results, portal vein diameter and mental state, and they were compared with those found in seven patients undergoing sclerotherapy of esophageal varices with comparable liver function (control group). Liver test results and levels of plasma insulin did not change in either group. Shunt significantly increased levels of fasting tyrosine, methionine, ornithine, arginine, histidine, ammonia and glucagon with respect to the control group; it also significantly decreased levels of leucine, valine, glucagon effectiveness and portal vein diameter. The elevation of levels of tyrosine, ammonia and the sum of arginine and ornithine was correlated directly with the increase in glucagon and inversely with the decline in glucagon effectiveness. Tyrosine increase was also correlated with the reduction of portal vein diameter. One shunted patient showed mild hepatic encephalopathy. Protein feeding did not worsen the mental state of patients before and after the operation. Surgery significantly increased the 5-hr response to the meal of gluconeogenic amino acids; its rise was again correlated with the changes in glucagon plasma levels and effectiveness. Although the absorptive levels of plasma ammonia were significantly higher 1 yr after surgery, its 5-hr response barely rose. In cirrhotic patients with a relatively preserved liver function, distal splenorenal shunt progressively worsened the fasting plasma profile of nitrogen compounds and the response to protein ingestion of gluconeogenic amino acids. The decline of portal blood flow and glucagon effectiveness may be causal factors. Despite this, the "cerebral" tolerance to a moderate oral load of protein was not reduced by surgery.
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PMID:Early and late changes in fasting and absorptive plasma amino acids and ammonia after distal splenorenal shunt in cirrhosis. 829 90

A total of 5473 pharmacological stimulation tests were carried out in 3143 children and subjected to statistical analysis. The mean chronological age of the children was 9 years 9 months (range 3 years to 16 years 6 months) and mean bone age was 7 years 6 months (range 2 years to 14 years). Nine pharmacological tests were used: (1) arginine (n = 625); (2) clonidine (n = 339); (3) insulin (n = 198); (4) ornithine (n = 162); (5) insulin and arginine (n = 203); (6) clonidine and betaxolol (n = 2003); (7) L-dopa (n = 685); (8) glucagon and propranolol (n = 443); and (9) glucagon and betaxolol (n = 815). Measurement of plasma growth hormone was always performed using the same method. The distribution of values in each test was of the gausso-logarithmic type. The results of the mean peak and the 95% confidence limit were as follows: (1) 10.2, 0.45; (2) 11.5, 0.7; (3) 11.8, 0.8; (4) 14.2, 1.2; (5) 14.3, 0.9; (6) 15.7, 1.1; (7) 19.8, 2.1; (8) 20.8, 2.3; (9) 21, 2.5. These results lead to the following conclusions: the specificity of these tests is low, the mean peak may vary two-fold from one test to another, and the percentage of peaks < 10 ng/ml ranges from 69% for test 1 to 29% for tests 8 and 9. The proportion of growth hormone deficiencies thus varies considerably according to the test used.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Statistical study of 5473 results of nine pharmacological stimulation tests: a proposed weighting index. 849 77

The rates of oxidation of arginine and ornithine that occurred through a reaction pathway involving the enzyme ornithine aminotransferase (EC 2.6.1.13) were determined using (14)C-labeled amino acids in the isolated nonrecirculating perfused rat liver. At physiological concentrations of these amino acids, their catabolism is subject to chronic regulation by the level of protein consumed in the diet. (14)CO(2) production from [U-(14)C]ornithine (0.1 mM) and from [U-(14)C]arginine (0.2 mM) was increased about fourfold in livers from rats fed 60% casein diets for 3-4 days. The catabolism of arginine in the perfused rat liver, but not that of ornithine, is subject to acute regulation by glucagon (10(-7) M), which stimulated arginine catabolism by approximately 40%. Dibutyryl cAMP (0.1 mM) activated arginine catabolism to a similar extent. In retrograde perfusions, glucagon caused a twofold increase in the rate of arginine catabolism, suggesting an effect of glucagon on arginase in the perivenous cells.
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PMID:Catabolism of arginine and ornithine in the perfused rat liver: effect of dietary protein and of glucagon. 1071 May 7

The effect of a "normal" (n = 8) and "high" (n = 6) protein intake (1 and 2.5 g x kg(-1) x day(-1), respectively) and of exercise on plasma amino acid (AA) concentrations, insulin, and glucagon concentrations was followed throughout a continuous 24-h period in adult male subjects at energy balance after six days on a standardized diet and exercise program. Subjects were fasting from 2100 on day 6 to 1200 on day 7 and then fed 10 identical meals hourly until 2100. Physical exercise was performed (46% maximal oxygen uptake) between 0830 and 1000 (fasting) and in a fed state (1600-1730) on each day. The normal-protein group showed fasting plasma AA concentrations that were higher (P < 0.05) than those for the high-protein group, except for leucine, methionine, and tyrosine. Glutamine, glycine, alanine, taurine, and threonine concentrations were distinctly higher ( approximately 30% or greater) throughout the 24-h period in subjects consuming the normal- vs. the high-protein diets. Exercise appeared to increase, although not profoundly, the plasma concentrations of amino acids except for glutamate, histidine, ornithine, and tryptophan. The profound diet-related differences in plasma AA concentrations are only partially explained by differences in the renal clearance of the amino acids. We speculate on the possible metabolic basis for these findings.
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PMID:Inverse relationship between protein intake and plasma free amino acids in healthy men at physical exercise. 1078 Sep 42


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