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)

When washed spleen slices from fed rats are incubated with 3 mm-[U-14C]glucose, the rate of glucose utilization (46.2 mumol/h per g dry wt.) is sufficient to account, theoretically, for 80% of the O2 consumption. Measurement of net lactate production, however, and the fate of the radioactive carbon, indicates that the contribution of glucose to the respiratory fuel of the tissue is only 25-30% whereas 60-70% of the glucose utilized is converted into lactate. At saturating glucose concentrations (above 5 mm) its contribution to the respiratory fuel of the slice is increased to a maximum value of 34-39%. Only 2% of the glucose utilized is metabolized via the oxidative steps of the pentose phosphate pathway. Starvation for 72 h marginally increases both the rate of glucose utilization (by 21%) and its net contribution to the respiratory fuel (by 29%). Insulin, glucagon, adrenaline and adenosine 3':5'-cyclic monophosphate have no significant effect on either the rate of glucose utilization or on the pattern of radioactive isotope distribution. The uptake of glucose is increased by only 20%, whereas the production of lactate doubles when slices are incubated under anaerobic conditions. In assessing the suitability of spleen slices for metabolic studies, the only serious major perturbation, compared with the freeze-clamped organ, is an elevated mitochondrial [NAD+]/[NADH] ratio (connected with increased endogenous NH3 production) that is partially restored to normal values on incubation with glucose. Equal proportions of erythrocytes and leucocytes are found in the washed spleen slice. Metabolic contributions of the constituent cell populations in the washed slice are calculated and it is concluded that lymphocytes account for the major part of the glycolytic metabolism (80-90%), whereas the contribution of erythrocytes is insignificant.
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PMID:Regulation of carbohydrate metabolism in lymphoid tissue. Quantitative aspects of [U-14C]glucose oxidation by rat spleen slices. 17 88

The effects of canola fat on digestion and metabolism were investigated by incorporating 0, 4.5, 9, 13.2, or 17.4% Jet-Sploded canola seed into a diet containing a 60:40 (DM) concentrate:forage ratio. The diets contained 16.5% CP, 30% alfalfa silage, and 10% whole-crop oat silage on a DM basis and were fed for ad libitum consumption as TMR to 10 ruminally cannulated Holstein cows in early lactation. Jet-Sploded canola seed supplementation did not change ruminal pH or NH3 N concentrations, but VFA concentrations declined with increasing level of inclusion. Apparent digestibilities of DM, OM, CP, NDF, and ADF were unaffected by level of inclusion of Jet-Sploded canola seed, but ether extract digestibility declined linearly, which resulted in similar ether extract absorption across the three diets supplemented with canola fat. Based on in sacco data, the percentages of ruminal digestion of OM and CP declined with increasing inclusion of Jet-Sploded canola seed. Plasma glucose and FFA concentrations tended to respond in a quadratic fashion, plasma insulin concentration declined linearly, and plasma glucagon and somatotropin concentrations were unaffected by dietary treatment. The results indicate that a positive productive response may be expected from dietary inclusion of about 5% Jet-Sploded canola seed, but the benefits of increased energy density associated with higher inclusion levels may be offset by reduced availability of energy in the rumen and decreased fat digestibility postruminally. The substantial effects of time postfeeding on ruminal fermentation and on concentrations of plasma hormone and metabolites in animals fed TMR demonstrate that infrequent sampling can result in misleading results and, thus, invalid interpretation of the influence of dietary fat on these parameters.
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PMID:Effect of canola fat on ruminal and total tract digestion, plasma hormones, and metabolites in lactating dairy cows. 131 41

The work was designed to study the effects of a meat meal on glomerular filtration rate (GFR), renal plasma flow (RPF), and plasma concentrations of glucagon, insulin, growth hormone, renin, aldosterone, total amino acids, and NH3 in healthy humans (H) as well as in patients with Child A liver cirrhosis (LC). The meat meal produced renal hyperaemia and hyperfiltration without changes in the filtration fraction. Fractional Na excretion in urine increased significantly after the meat meal only in LC. Hyperinsulinaemia and hyperglucagonaemia were seen at baseline in LC and were not affected by the meat meal, whereas in H glucagon concentration increased significantly over baseline within 30 min from the meat meal and insulin within 60 min. Growth hormone concentration was normal at baseline in LC and increased significantly 120-180 min after the meal, whereas it was not affected in H. Renin and aldosterone were stable in both H and LC. Plasma amino acid concentration began to increase 60 min after the meat meal, when hyperfiltration was present. The data indicate that in human Child A cirrhosis of the liver renal haemodynamic response to a meat meal is independent of changes in glucagon.
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PMID:Glucagon-independent renal hyperaemia and hyperfiltration after an oral protein load in Child A liver cirrhosis. 155 40

1. Glutaminase activity was measured in primary cultures of hepatocytes. 2. Enzyme activity decreased markedly after 24-40 h in culture, and this loss of activity was accompanied by loss of enzyme protein. 3. The loss of activity was delayed by high concentrations of glutamine, and was abolished by the continuous presence of NH4Cl in the culture medium. 4. In cells from rats fed on high-carbohydrate protein-free diet, glutaminase activity was increased by glucagon, but not by dexamethasone. This induction was observed only in the continuous presence of NH3 or high concentrations of glutamine. 5. It is concluded that NH3 and glutamine are essential for the stabilization and induction of glutaminase activity in hepatocytes. The inactivation of glutaminase in hepatocytes and in vivo under certain conditions may be due to lack of NH3 in the extracellular medium.
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PMID:Glucagon and ammonia influence the long-term regulation of phosphate-dependent glutaminase activity in primary cultures of rat hepatocytes. 200 Dec 24

The aim of this study was to evaluate the contribution of gluconeogenesis from amino acids in the development of fasting and absorptive hyperammonemia in cirrhosis. Somatostatin (SRIF), which is known to inhibit the hepatic disposal of gluconeogenic amino acids, was administered in a continuous infusion (500 micrograms/h) for 90 min before and 5 h after a protein meal (240 g of meat) in 11 overnight fasting patients. Plasma glucagon, insulin, gluconeogenic amino acids (GAA: alanine, serine, glycine, and threonine) and ammonia (NH3) were evaluated before the infusion, immediately before, and at 1, 3, and 5 h after the meal. As control study, the same protocol was randomly repeated in a different day with saline infusion. During the latter, a direct correlation was found between fasting glucagon and ammonia (r = 0.68; p less than 0.05). Fasting glucagon, insulin, and NH3 did not change, whereas alanine (p less than 0.05) and the GAA sum decreased (p less than 0.01). When SRIF was infused, fasting glucagon (p less than 0.05), insulin (p less than 0.05), and NH3 (p less than 0.05) decreased. Alanine did not change, and GAA sum increased (p less than 0.02). No correlations were found by plotting changes in glucagon or GAA sum and NH3. After the meal, SRIF infusion abolished the plasma response of glucagon and markedly reduced that of insulin, so that their area under the curve (AUC0-5) were reduced (p less than 0.005, for both), with respect to control study. Moreover, the AUC0-5 of alanine (p less than 0.005) and GAA sum (p less than 0.005) were increased, suggesting a reduced disposal of these compounds. In spite of this, the meal-induced early increase and the AUC0-5 of plasma NH3 observed during SRIF and saline infusion did not differ. Our results do not confirm the importance of gluconeogenesis from alpha-amino-nitrogens in determining the fasting ammonemia of cirrhosis, and suggest that this metabolic pathway does not significantly influence the protein meal-induced exacerbation of plasma ammonia.
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PMID:Role of gluconeogenesis from amino acids in determining fasting and absorptive levels of plasma ammonia in cirrhosis. 289 85

The effects of subclinical NH3 toxicity on circulating and regulatory hormone concentrations were investigated in seven Hereford steers. Ammonium chloride (NH4Cl) was infused via a right jugular vein catheter at a rate of 12 mumol NH4Cl.kg BW-1.min-1 for 240 min. This was preceded (PRE) and followed (POST) by saline infusions of 120 and 180 min, respectively. Blood samples were taken at 20-min intervals via a left jugular vein catheter. Metabolite and hormone concentrations during NH4Cl and POST periods were compared to PRE values using the Student's t-test procedure. Plasma NH3 was elevated rapidly (P less than .001) and peaked at 503 micrograms/dl 220 min into NH4Cl infusion. Plasma urea-N and glucose increased (P less than .001) 39 and 12%, respectively, during NH4Cl infusion and remained elevated 180 min POST. Whole blood L-lactate concentrations peaked (P less than .05) at 18% above PRE between 160 and 240 min into the NH4Cl infusion and gradually returned to PRE values, whereas pyruvate levels were not altered (P greater than .10). Plasma nonesterified fatty acids peaked (P less than .001) at 94% above PRE levels 40 min into NH4Cl infusion, thereafter declining to PRE concentrations. Whole blood acetoacetate and beta-hydroxybutyrate concentrations were not altered (P greater than .10) by NH4Cl administration. Plasma insulin concentration decreased (P less than .05) 26 to 46% during NH4Cl infusion and increased (P less than .05) 89 to 122% during POST. Plasma glucagon levels were not altered by NH4Cl infusion, so molar insulin:glucagon ratio changes resembled those of insulin. Plasma epinephrine, norepinephrine and dopamine did not vary (P greater than .10) with treatment. These results support the hypothesis that the hyperglycemia observed during hyperammonemia may result from an under-utilization of glucose by insulin-sensitive tissues.
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PMID:Subclinical ammonia toxicity in steers: effects on blood metabolite and regulatory hormone concentrations. 306 22

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 aim of this paper is to elucidate the cause of death after 90 min of normothermic partial (2/3) ischemia of the liver and to examine the effects of glucagon, somatostatin, insulin, prednisolone and oral administration of polymyxin B (PB). The animals 24 hr after partial ischemia for 90 min were divided into two groups; namely, animals with normal appearance and those with moribund state. There were no significant differences in the plasma level of S-GOT, S-GPT, amino acids, NH3 or insulin, or in morphometrically estimated volume ratio of necrotic hepatocytes between the two groups of rats. The blood glucose level, however, was significantly decreased (31 +/- 28 mg/100 ml, n = 6) in the moribund rats with a higher incidence of positive Limulus gelation tests as compared with the rats with normal appearance (149 +/- 19, n = 5). The 1-day and 1-week survival rates of the animals were 42/62 (69%) and 32/61 (53%), respectively. A glucagon injection (1.5 mg/kg, after ischemia) was effective to elevate the 1-day survival rate (14/14), but failed to increase the 1-week survival rate (11/14). On the other hand, a somatostatin injection (100 micrograms/kg, after ischemia) or PB treatment (15 mg/kg/day x 5-9, before ischemia) succeeded to increase the 1-week survival rate (20/22 p less than 0.01 and 17/17 p less than 0.01, respectively), although no significant amelioration in transaminase levels or volume ratio of necrosis was demonstrated. It could be seen that a moribund state after partial ischemia was accompanied by severe hypoglycemic shock, and that the injection of somatostatin after ischemia or the annihilation of gram-negative bacteria by means of oral administration of polymyxin B before ischemia prevented the occurrence of the hypoglycemic shock.
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PMID:Postischemic liver damage in rats: effect of some therapeutic interventions on survival rate. 629 17

Investigations were made on the effects of catecholamine (Cat) infusions with and without ammonia (NH3) on plasma and brain amino acids (AA) and brain neurotransmitters in dogs. Groups of four dogs were infused for 5 h with epinephrine (E), epinephrine + norepinephrine (E + NE), epinephrine + norepinephrine with NH3 during h 4 and 5 (E + NE + NH3), epinephrine + norepinephrine + tryptophan with NH3 during h 4 and 5 (T + E + NE + NH3), or saline (C). Cat decreased (P less than 0.05) plasma Gly, Thr, Lys, Pro, Val, Ser, Arg, Leu, Trp, Phe, Asn, Tyr, Met, Ile, Cit, and Asp. The decreases at h 3 for all were to a mean of 45% of 0 h and were associated with no changes in plasma insulin or glucagon. Cat increased plasma Tau and Orn. Of the most abundant brain AA (82% of total), E + NE + NH3 had no effect (GABA, Asp, Gly, Ala, p-ethanolamine) or increased (Glu, Gln, Tau) brain levels. These AA were unchanged by Cat alone. Of the remaining brain AA, most were decreased by Cat (7 of 16, P less than 0.05) and E + NE + NH3 increased brain Trp but had no effect on brain serotonin, 5-hydroxyindoleacetic acid, or NE. Cat changed plasma AA in a way similar to changes produced by NH3 infusion and seen with hepatic insufficiency due to portacaval shunts and nitrosamine-induced pathology. Cat reduced brain AA levels, and this was partially restored by NH3.
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PMID:Effects of catecholamines and ammonia on plasma and brain amino acids in dogs. 646 11

Glucagon, a potent inducer of urea cycle enzymes, was administered subcutaneously, at a dose of 0.5 mg once a day, for 7 days to two citrullinemic patients. During this period, plasma NH3 levels in case 1 decreased significantly (P < 0.05 compared to levels before administration) and daily urinary excretion of urea N increased significantly (P < 0.05). For 1 week after the cessation of administration, the daily urinary excretion of urea N was significantly higher than the level before administration (P < 0.05), the plasma citrulline level during glucagon administration was lower than that before administration. In case 2, glucagon administration also decreased the plasma NH3 level (although the decrease was not statistically significant), and significantly increased daily urinary excretion of urea N (P < 0.05 compared to levels before administration). For 1 week after the cessation of glucagon administration the plasma citrulline level was significantly lower than that before administration (P < 0.05). These results indicate that glucagon significantly increases the urinary excretion of urea in the late onset form of argininosuccinate synthetase deficiency and that it may also decrease plasma NH3 levels in some patients with the deficiency.
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PMID:Effects of glucagon on urinary excretion of urea and on plasma ammonia level in argininosuccinate synthetase deficiency. 819 93


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