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 effects of subcutaneous injection of cysteamine (2-mercaptoethylamine, 300 mg/kg) were investigated in 5-6 week-old chickens. 2. In the short term (1 hr), cysteamine increased plasma levels of glucose, free fatty acids and insulin, and decreased that of alpha-amino non protein nitrogen. 3. In a longer term (17-24 hr), cysteamine increased the plasma level of glucose, did not modify those of alpha-amino non protein nitrogen, insulin and glucagon and decreased that of free fatty acids. 4. The disposal of an oral glucose load was impaired and the glucose-induced inhibition of pancreatic glucagon and stimulation of insulin release were blunted 17 hr after cysteamine administration. 5. Therefore, cysteamine exerts multiple effects on chicken pancreatic islet cells.
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PMID:Effects of cysteamine administration on plasma concentration of metabolites, pancreatic glucagon and insulin in the chicken. 197 75

Metabolic changes in six severely affected tetanus patients suffering from characteristic labile hypertension (maximum systolic blood pressure greater than 200 mmHG, maximum diurnal change in systolic pressure greater than 100 mmHg) were investigated. Daily urinary excretion of urea nitrogen increased gradually from the onset of opisthotonus, reached a peak value (10.4 to 15.4 g/m2) in 8 to 20 days, and decreased subsequently. Average cumulative excretion in 30 days reached 239.6 +/- 32.7 g/m2. Urine catecholamine excretion was elevated in each patient and remained elevated during this period. Plasma cortisol and glucagon concentrations were not increased markedly except in a case complicated other systemic bacterial infection. Increased protein catabolism in these patients could not be explained by the metabolic effects of 'stressed hormones' alone, and neurologic factors must be considered.
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PMID:Metabolic changes in patients severely affected by tetanus. 198 40

The effects of intravenous infusion of 17 amino acids, each at a dose of 3 mmol/kg over 30 min, on the secretion of insulin, glucagon, and growth hormone (GH) were studied in 6 castrated male sheep. Insulin-like growth factor I (IGF-I) secretion was also studied using eight of the amino acids. Plasma alpha-amino nitrogen reached a peak at 30 min followed by a gradual decrease thereafter. The greatest increase was obtained using aspartic acid and the smallest with methionine, responses to the remaining amino acids lying between these two. Leucine was the most effective amino acid in stimulating insulin secretion but did not produce any increase in glucagon and GH secretion. Alanine, glycine, and serine induced a greater enhancement of both glucagon and insulin secretion than other amino acids. No amino acid was able to specifically stimulate glucagon secretion without also increasing insulin or GH secretion. With regard to insulin and glucagon secretion, amino acids could be divided into groups according to their R groups. Neutral straight-chain amino acids stimulated both insulin and glucagon secretion, with a greater secretory response to shorter C-chain amino acids. Branched-chain amino acids tended to enhance insulin and suppress glucagon secretion. Acidic amino acids caused an increase in GH secretion. Aspartic acid caused the strongest stimulation of GH secretion, exceeding that induced by arginine. No changes in plasma IGF-I were brought about by any of the amino acids tested.
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PMID:Effects of intravenous infusion of 17 amino acids on the secretion of GH, glucagon, and insulin in sheep. 198 90

Both albuminuria (UalbV) and albumin synthesis (AlbSyn) are modulated by dietary protein in nephrotic rats, but the agent(s) linking diet to altered UalbV and AlbSyn is unknown. Others have reported that branched-chain amino acids (BCAA) cause neither increased renal blood flow nor glomerular filtration rate (GFR) normally induced by dietary protein nor increased blood glucagon thought to be necessary for protein-mediated effects on renal hemodynamics. The effect of BCAA on UalbV is unknown. Because BCAA increase AlbSyn in tissue culture and after a fast, it is possible that feeding BCAA may increase AlbSyn but not UalbV in nephrosis. Nephrotic rats were fed either 8.5% casein (LP); 21% casein (NP); 8.5% casein supplemented with valine, leucine, and isoleucine to the total amount provided by a 21% casein diet (2.37%) (LBC); or 8.5% casein plus 12.5% BCAA providing a diet isonitrogenous to 21% casein (HBC). UalbV and AlbSyn were significantly greater in NP compared with LP, LBC, or HBC and were the same in the latter three groups. Glucagon was infused into nephrotic rats fed 8.5% casein either subcutaneously or intraperitoneally in quantities sufficient to increase plasma levels to over 10 times control but had no effect on UalbV. The ability of dietary protein to increase AlbSyn or UalbV is not a result of total alpha-amino nitrogen intake but is a result of the specific amino acid composition of the diet and must result entirely from the effect of one or more non-BCAA. Increased blood glucagon alone has no effect on UalbV.
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PMID:Branched-chain amino acids augment neither albuminuria nor albumin synthesis in nephrotic rats. 199 10

The effects of i.v. glucagon-like peptide-1-(7-36)amide (GLP-1; 10 micrograms) on starved sheep given an i.v. glucose load (5 g) were studied. Plasma insulin concentrations rose significantly more after glucose administration in fed than in starved sheep. Giving GLP-1 to starved sheep increased the insulin response to the glucose load. The rise in plasma insulin concentrations in starved sheep given GLP-1 was similar to that observed in fed sheep. Plasma glucose concentrations returned to normal values more quickly in the starved sheep given GLP-1 than in starved sheep not given gut hormone. Plasma concentrations of free fatty acid, urea and alpha-amino nitrogen decreased more quickly following glucose administration in starved sheep given GLP-1 than in those not given GLP-1. The data suggest a role for GLP-1 in regulating plasma insulin concentrations and hence metabolism in ruminant animals. The possible role of gut hormones in ruminants is discussed.
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PMID:Effects of truncated glucagon-like peptide-1 on the responses of starved sheep to glucose. 203 Mar 30

The effect of metabolic acidosis (MA) on amino acid and keto acid metabolism was studied in fourteen patients with chronic renal failure (CRF) under the low protein diet (0.6-0.8 g/kgBW). The comparative study of five patients with renal tubular acidosis was carried out. Each patient was investigated before [MA(+)period] and after correction with sodium bicarbonate administration lasting 10 days [MA(-)period]. The correction of MA improved nitrogen balance and elevated plasma branched-chain amino acids (BCAA), keto acids (BCKA), glutamine and alanine concentrations. No effect was however, observed in change of plasma insulin and glucagon. Oral administration of the keto-analogues of BCKA [0.1 g/kgBW of alpha-ketoisovalerates (KIV) and alpha-keto-isocaproic acid (KIC)] is made for the purpose of investigating the change in the metabolic conversion rate to amino acids. As a result, MA (+) suppressed an increase in plasma KIV and KIC concentrations. Moreover, an increase in plasma valine and leucine concentrations were suppressed by MA (+). These results suggested that MA stimulates BCKA oxidation and suppresses the protein sparing effect of leucine and KIC, and accelerates the catabolism in CRF under the low protein diet. The correction of MA is ineffective in severe renal failure (serum creatinine above 10.0 mg/dl), because the other uremic factors appear to be affecting protein and amino acid metabolism. Therefore, it might be concluded that MA should be corrected at an earlier stage of CRF.
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PMID:[The effect of metabolic acidosis on amino acid and keto acid metabolism in chronic renal failure]. 205 49

Previous work in this laboratory has shown that muscle malonyl-CoA, the inhibitor of carnitine palmitoyltransferase I (CPT I), decreased during exercise. Hepatic malonyl-CoA content decreases when glucose availability decreases such as during fasting or when the glucagon-to-insulin ratio increases such as during prolonged exercise or in response to insulin deficiency. To investigate the effect of glucose infusion on muscle malonyl-CoA during exercise, male rats were anesthetized (pentobarbital via venous catheters) at rest or after running (21 m/min, 15% grade) for 30 or 60 min. During exercise rats were infused with either glucose (0.625 g/ml) or saline at a rate of 1.5 ml/h. Gastrocnemius muscles and liver samples were frozen at liquid nitrogen temperature. Muscle malonyl-CoA decreased from 1.24 +/- 0.06 to 0.69 +/- 0.05 nmol/g with glucose infusion and to 0.43 +/- 0.04 nmol/g with saline infusion during 60 min of exercise. In the liver, glucose infusion prevented the drop in malonyl-CoA. This indicates that glucose infusion attenuates the progressive decline in muscle malonyl-CoA and prevents the decline in liver malonyl-CoA during prolonged exercise.
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PMID:Effect of glucose infusion on muscle malonyl-CoA during exercise. 205 26

The increased fuel demands of the working muscle necessitate that metabolic processes within the liver be accelerated accordingly. The sum of changes in hepatic glycogenolysis and gluconeogenesis are closely coupled to the increase in glucose uptake by the working muscle, due to the actions of the pancreatic hormones. The exercise-induced rise in glucagon and fall in insulin interact to stimulate hepatic glycogenolysis, whereas the increase in gluconeogenesis is determined primarily by glucagon action. The increment in gluconeogenesis is caused by increases in hepatic gluconeogenic precursor delivery and fractional extraction as well as in the efficiency of intrahepatic conversion to glucose. Glucagon stimulates the latter two processes. Epinephrine may become important in the regulation of hepatic glucose production during prolonged or heavy exercise when its levels are particularly high. On the other hand, there is no evidence that hepatic innervation is essential for the rise in hepatic glucose production during exercise. Nonesterified fatty acid (NEFA) delivery to, uptake of, and oxidation by the liver are accelerated during prolonged exercise, resulting in an increase in ketogenesis. The rate of the first two of these processes is largely determined by factors that stimulate fat mobilization. The third step is regulated by both NEFA delivery to and glucagon-stimulated fat oxidation within the liver. The increase in hepatic fat oxidation produces energy that fuels gluconeogenesis. The shuttling of amino acids to the liver provides carbon-based compounds that are used for gluconeogenesis, transfers nitrogen to the liver, and supplies substrate for protein synthesis. During exercise, metabolic events within the liver, which are regulated by hormone levels and substrate supply, integrate pathways of carbohydrate, fat, and amino acid metabolism. These processes function to provide substrates for muscular energy metabolism and conserve carbon in glucose and nitrogen in protein.
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PMID:Hepatic fuel metabolism during muscular work: role and regulation. 205 58

In diabetes mellitus amino nitrogen is lost from organs and excreted as urea. Traditionally it has been assumed that the only explanation of this phenomenon was lack of insulin. The blood amino acid concentration in diabetic patients is, however, reduced, which suggests that the hepatic uptake of amino acids is accelerated. Glucagon accelerates the hepatic uptake and conversion of amino nitrogen into urea nitrogen, and hyperglucagonaemia is present in diabetes. This survey describes the significance of hyperglucagonaemia in the abnormal diabetic nitrogen metabolism. Rats with experimental diabetes and hyperglucagonaemia, given the same amount of food as controls, double the urinary excretion of urea-N within 4 days. This increase can be completely normalized by an intensive insulin treatment regimen, which normalises the hyperglucagonaemia as well. Selective hyperglucagonaemia in otherwise optimally insulin treated diabetic rats raises the urinary urea-N excretion by one third, also within 4 days. The kinetics of urea synthesis in experimental diabetes is changed towards an increased maximum rate, but only after 14 days, so this alone cannot explain the increased urea excretion. Constant hyperglucagonaemia increases the spontaneous rate of urea synthesis within 2 days. In uncontrolled diabetes nitrogen is lost from most organs, and most is lost from muscles. Selective hyperglucagonaemia in insulin treated diabetic rats leads to a loss of muscle nitrogen of about one third of that seen in uncontrolled diabetes. It is suggested that he glucagon induced loss of muscle nitrogen is due to an increased flux of amino nitrogen from muscle to liver.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Importance of glucagon for nitrogen loss in diabetes--via an accelerated hepatic conversion of amino nitrogen to urea nitrogen. 206 Mar 19

To determine influences of insulin and body condition on follicular growth, prepuberal gilts (n = 16) treated with pregnant mare's serum gonadotropin (PMSG) were used in a 2 X 2 factorial experiment with main effects of insulin (0 or .4 IU/kg every 12 h beginning at 1800 on the day before PMSG) and backfat depth (moderate, 25 +/- .8; high, 32 +/- .7 mm; P less than .0001). Body weights were similar. Blood sampling was at 6-h intervals for analyses of LH, FSH, growth hormone (GH), glucagon, cortisol, insulin, insulin-like growth factor-I (IGF-I), plasma urea nitrogen (PUN), nonesterified fatty acids (NEFA), testosterone, estradiol-17 beta, and progesterone. Ovaries were removed 75 h after PMSG treatment, and visible small (less than or equal to 3 mm), medium (4 to 6 mm), large (greater than or equal to 7 mm), and macroscopically atretic follicles were counted. Administration of insulin increased IGF-I in fluid of medium follicles (108.8 vs 60.7 ng/ml; SEM = 13.3; P less than .05). Neither insulin nor fatness affected hCG binding by granulosa cells (12.5 +/- 1.6 ng/10(6) cells) or numbers of large (16.7 +/- 2.6) and medium (10.4 +/- 2.3) follicles. However, insulin increased the number of small follicles (58.9 vs 29.9; SEM = 9.7; P less than .05) and reduced the number of atretic follicles (3.8 vs 11.3; SEM = 1.1; P less than .05). The predominant effect of insulin on reducing number of atretic follicles was in the small size class (.6 vs 6.9; SEM = .6, P less than .01). Follicular fluid estradiol and progesterone were not affected by treatments; however, testosterone concentrations in large follicles were lower in gilts with higher backfat (32.5 vs 59.9 ng/ml; SEM = 4.0; P less than .05). Systemic LH, FSH, glucagon, cortisol, PUN, NEFA, estradiol, and testosterone were not affected by insulin or level of feeding. However, GH was lower in gilts that had higher backfat (overall average of 3.2 vs 2.8 ng/ml; SEM = .1; P less than .05). Insulin reduced atresia and altered intrafollicular IGF-I independently of body condition and without sustained effects on other hormones.
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PMID:Effects of exogenous insulin and body condition on metabolic hormones and gonadotropin-induced follicular development in prepuberal gilts. 206 18


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