Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.3.9 (glucose-6-phosphatase)
3,081 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum activity has been measured in three of the key enzymes in the gluconeogenic pathway in rats subjected to experimental hepatotoxicity after intraperitoneal administration of carbon tetrachloride. The levels of phosphoenolpyruvate carboxykinase (PEPCK) and fructose-1,6-biphosphatase (FBPase) showed a similar behavior to the transaminase (AST and ALT), increasing markedly with respect to the controls at 12 h after administration of the poison, reaching their maximum peak of activity at between 24 and 36 h, and returning to normal values at 96 h. The activity of glucose-6-phosphatase was not significantly modified throughout the treatment. These results seem to demonstrate that the determination of the serum activity of PEPCK and FBPase could be a sensitive and specific marker of hepatic cytolysis.
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PMID:Serum activity of the key gluconeogenic enzymes in carbon-tetrachloride-induced experimental hepatotoxicity. 196 85

In order to evaluate the usefulness of key gluconeogenic enzymes, in relation to the markers commonly used (alkaline phosphatase and gamma-glutamyl transpeptidase) for the diagnose of cholestasis the serum activity of phosphoenolpyruvate carboxykinase, fructose 1,6-bisphosphatase and glucose-6-phosphatase has been measured in rats with bile-duct ligation. Among the gluconeogenic enzymes studied only phosphoenolpyruvate carboxykinase activity increased significantly in the first 48 hours after cholestasis, decreasing thereafter to normal values. Both alkaline phosphatase and gamma-glutamyl transpeptidase activities showed a very significant increase which persisted throughout the experiment. These results seem to indicate that in spite of the high organ specificity of these enzymes they do not appear to be useful for the diagnosis of cholestasis.
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PMID:Evaluation of key gluconeogenic enzymes in experimental biliary obstruction. 198 72

Twenty obese and 20 lean LA/N-cp male rats and 20 male Sprague-Dawley rats were fed a diet containing either 54 percent sucrose or starch for six weeks. After a 14-16 hour fast, rats were killed. Liver and kidney enzyme activities were determined in the LA/N-cp rats while plasma urea and selected amino acids were determined in all rats. Liver glucose-6-phosphatase (G6PASE), fructose-1,6-bisphosphatase (FBPASE), phosphoenolpyruvate carboxykinase (PEPCK), glucose-6-phosphate dehydrogenase (G6PDH), 6-phosphogluconate dehydrogenase (6PGDH), malic enzyme (ME), glucokinase (GK), pyruvate kinase (PK), phosphofructokinase (PFK), glutamic-oxaloacetic-transaminase (GOT), glutamic-pyruvic transaminase (GPT), arginase (ARGASE), arginine-synthase (ARG-SYN) and ornithine transcarbamylase (OTC) levels were significantly affected by phenotype (obese greater than lean). All the above changes in enzyme levels were exaggerated by sucrose-feeding with the exception of PK, PFK, GOT, GPT, ARGASE and ARG-SYN. Kidney cortex G6PASE, PEPCK and ARGASE activities were higher in the obese rats as compared to the lean littermates. Sucrose feeding resulted in higher cortex G6PASE, FBPASE and PEPCK as compared to starch-fed rats. A phenotype effect was noted with plasma glutamate, urea, leucine, isoleucine and valine (obese greater than lean) and a diet effect was seen with aspartate, phenylalanine, leucine and valine (sucrose greater than starch) concentration. Sprague-Dawley rats had higher plasma urea and lower alanine than lean LA/N-cp males. Metabolic obesity in the LA/N-cp rat appears to involve an elevated capacity for pathways of glycolysis, gluconeogensis, lipogenesis and amino acid catabolism in the liver.
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PMID:Effect of dietary carbohydrate on liver and kidney enzyme activities and plasma amino acids in the LA/N-cp rat. 204 12

Male Sprague-Dawley rats (240-245 g) were dosed ip with 5, 15, 25, or 125 micrograms/kg -,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in corn oil. Ad libitum-fed and pair-fed controls received vehicle (4 ml/kg) alone. Two or 8 days after dosing five rats of each group were sacrificed, their livers removed and assayed for the activities of three gluconeogenic enzymes [phosphoenol-pyruvate carboxykinase (PEPCK; EC 4.1.1.32), pyruvate carboxylase (PC; EC 6.4.1.1), and glucose-6-phosphatase (G-6-Pase, EC 3.13.9)], and one glycolytic enzyme [pyruvate kinase (PK; EC 2.7.1.40)] by established procedures. The activity of PK was not affected by TCDD at either time point. The activity of G-6-Pase tended to be decreased in TCDD-treated animals, as compared to pair-fed controls, but the decrease was variable without an apparent dose-response. The activity of PEPCK was significantly decreased 2 days after dosing, but a clear dose-response was apparent only at the 8-day time point. Maximum loss of activity at the highest dose was 56% below pair-fed control levels. PC activity was slightly decreased 2 days after TCDD treatment and displayed statistically significant, dose-dependent reduction by 8 days after dosing with a 49% loss of enzyme activity after the highest dose. It is concluded that inhibition of gluconeogenesis by TCDD previously demonstrated in vivo is probably due to decreased activities of PEPCK and PC. The data also support the prevailing view that PEPCK and PC are rate-determining enzymes in gluconeogenesis.
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PMID:Key enzymes of gluconeogenesis are dose-dependently reduced in 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-treated rats. 205 51

Treatment of rats with diazinon (40 mg/kg, i.p.) resulted in hyperglycaemia and depletion of glycogen from the brain and peripheral tissues two hours after administration. The activities of glycogen phosphorylase and phosphoglucomutase were significantly higher in the brain and liver; that of glucose-6-phosphatase was not altered. The activities of the glycolytic enzymes hexokinase and lactate dehydrogenase were increased only in the brain. The cholinesterase activity in the brain was reduced by treatment with diazinon. The activities of the hepatic gluconeogenic enzymes fructose 1,6-diphosphatase and phosphoenolpyruvate carboxykinase were significantly increased. The lactate level was increased in the brain and blood, whereas that of pyruvate was not changed. The activity of glucose-6-phosphate dehydrogenase was not changed to any major extent. Cholesterol and ascorbic acid contents of adrenals were depleted in diazinon-treated animals. The changes were pronounced after intraperitoneal administration of 40 mg/kg diazinon, they were slight but significant after 20 mg/kg, and absent after 10 mg/kg. Hyperglycaemia and changes in carbohydrate metabolism were abolished by adrenalectomy suggesting possible involvement of adrenals.
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PMID:The role of adrenals in diazinon-induced changes in carbohydrate metabolism in rats. 209 50

1. The regulation of renal gluconeogenesis was studied in rats made septic by a caecal ligation and puncture technique. 2. Blood glucose concentrations were not markedly different in septic rats, but lactate, pyruvate and alanine concentrations were markedly increased, compared with sham-operated rats. Conversely, blood ketone body concentrations were significantly decreased in septic rats. Both plasma insulin and glucagon concentrations were markedly elevated in response to sepsis. 3. The maximal activities of glucose-6-phosphatase (EC 3.1.3.9), fructose-1,6-bisphosphatase (EC 3.1.3.11), pyruvate carboxylase (EC 6.4.1.1) and phosphoenolpyruvate carboxykinase (EC 4.1.1.49) were markedly decreased in kidneys obtained from septic rats, suggesting diminished renal gluconeogenesis. 4. Renal concentrations of lactate, pyruvate and other gluconeogenetic intermediates were markedly elevated in septic rats, whereas those of acetyl-CoA and fructose 2,6-bisphosphate were decreased and unchanged, respectively. 5. The rate of gluconeogenesis from added lactate, pyruvate and glycerol was decreased in isolated incubated renal tubules from septic rats. 6. Sepsis decreased the arteriovenous concentration difference for glucose, lactate, and alanine. Septic rats showed decreased net rates of glucose production and net rates of removal of lactate and alanine as compared with sham-operated controls. 7. It is concluded that the diminished capacity for renal gluconeogenesis in septic rats could be the result of changes in the maximal activities or regulation of key non-equilibrium gluconeogenic enzymes or both, but the effect of other factors (e.g. toxins) has not been excluded.
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PMID:Metabolic regulation of renal gluconeogenesis in response to sepsis in the rat. 217 16

Treatment with diazinon (40 mg/kg, i.p.) resulted in hyperglycemia and depletion of glycogen from cerebral and peripheral tissues 2 hr after its administration in rats. The activities of the glycogenolytic enzymes glycogen phosphorylase and phosphoglucomutase were increased significantly in brain and liver, whereas that of glucose-6-phosphatase was not altered. The activities of the glycolytic enzymes hexokinase and lactate dehydrogenase were increased only in the brain. The cholinesterase activity of the brain was reduced by treatment with diazinon. The activities of the hepatic gluconeogenic enzymes fructose 1,6-diphosphatase and phosphoenolpyruvate carboxykinase were also increased significantly in diazinon-treated animals. The level of lactate was increased in brain and blood, whereas that of pyruvate was not changed. The activity of glucose-6-phosphate dehydrogenase was not changed significantly. The cholesterol and ascorbic acid contents of adrenals were depleted in diazinon-treated animals. The hyperglycemia and changes in carbohydrate metabolism were abolished by adrenalectomy, suggesting the possible involvement of the adrenals in the induced changes in diazinon-treated animals.
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PMID:Modification of diazinon-induced changes in carbohydrate metabolism by adrenalectomy in rats. 234 75

Treatment with diazinon resulted in hyperglycaemia and depletion of glycogen from cerebral and peripheral tissues 2 h after its administration in rats; the changes were maximal after 40 mg/kg diazinon, administered intraperitoneally. The activities of glycogen phosphorylase and phosphoglucomutase were significantly increased in brain and liver, while that of glucose-6-phosphatase was not altered. The activities of the glycolytic enzymes hexokinase and lactate dehydrogenase were increased only in brain. The cholinesterase activity of the brain was reduced by treatment with diazinon. The activities of hepatic gluconeogenic enzymes (fructose 1,6 diphosphatase and phosphoenolpyruvate carboxykinase) were also significantly increased in diazinon-treated animals. The level of lactate was increased in brain and blood while that of pyruvate was not changed. The activity of glucose-6-phosphate dehydrogenase was not significantly changed. Cholesterol and ascorbic acid contents of adrenals were depleted in diazinon-treated animals. Adrenalectomy abolished the hyperglycaemia and changes in carbohydrate metabolism, suggesting the possible involvement of adrenals in the induced changes in diazinon-treated animals.
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PMID:Effect of adrenalectomy on diazinon-induced changes in carbohydrate metabolism. 281 1

The capacity for gluconeogenesis in the isolated amphibian retina was found to be approx. 70-fold greater with lactate than with glutamate as the gluconeogenic precursor, 1426 versus 21 pmol of glucose incorporated into glycogen/h per mg of protein. It was also found that 11-15% of the glucosyl units in glycogen are derived from C3 metabolites of the glycolytic pathway, suggesting that lactate is recycled within the retina. In concert with these metabolic observations, a full complement of the gluconeogenic enzymes was detected in retinal homogenates. These included: glucose-6-phosphatase, fructose-1,6-bisphosphatase, acetyl-CoA-dependent pyruvate carboxylase and phosphoenolpyruvate carboxykinase. Agents that regulate the rate of gluconeogenesis in hepatic tissue were tested on the retina. At concentrations of glutamate and lactate that are presumed to be relevant physiologically, it was found that vasoactive intestinal peptide, ionophore A23187 and elevated [K+] each enhanced the rate of gluconeogenesis in Ringer containing 50 microM-glutamate, whereas in Ringer containing 8.5 mM-lactate these agents inhibited the rate of gluconeogenesis. Further, it was found that the classic gluconeogenic hormone glucagon inhibited gluconeogenesis in both glutamate- and lactate-containing Ringer. Retinal energy metabolism was found to be altered in lactate-containing Ringer, in that lactate production was suppressed completely. In addition, glycogen metabolism appeared to be dependent on increased cytosolic Ca2+ and was insensitive to increased retinal cyclic AMP.
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PMID:Gluconeogenesis in the amphibian retina. Lactate is preferred to glutamate as the gluconeogenic precursor. 290 49

Glucose transport and metabolism, and the effect of insulin thereon, was studied using suspensions of rat renal tubules enriched in the proximal component. [U-14C]Glucose oxidation is a saturable process (Km 3.1 +/- 0.2 mM; Vmax 14 +/- 0.2 mumole 14CO2 formed/g tissue protein per h). Glucose oxidation and [14C]lactate formation from glucose are inhibited in part by phlorizin and phloretin: the data suggest that the rate-limiting entry of glucose into the cell metabolic pool occurs by both the Na-glucose cotransport system (at the brush border) and the equilibrating, phloretin-sensitive system (at the basal-lateral membrane). Raising external glucose from 5 to 30 mM markedly increases aerobic and anaerobic lactate formation. Gluconeogenesis from lactate is not affected by variations of glucose concentrations. 24 h after streptozotocin administration, aerobic lactate formation is enhanced, as is the uptake of methyl alpha-D-glucoside by the tubules, while anaerobic glycolysis is depressed. Streptozotocin treatment (ST) increases both the Km and Vmax of glucose oxidation; gluconeogenesis and lactate oxidation are not affected. The effect of streptozotocin treatment on lactate formation are abolished by 1 mU/ml insulin. Streptozotocin treatment increases tissue hexokinase activity, decreases glucose-6-phosphatase, but has no significant effect on fructose-1,6-diphosphatase; phosphoenolpyruvate carboxykinase and pyruvate dehydrogenase. The data demonstrate fast streptozotocin-induced changes in cellular enzymes of carbohydrate metabolism. The enhancing effect of streptozotocin on methyl alpha-glucoside uptake is transient: 8 days after administration of the agent, no significant difference from controls is found. It is concluded that under the given experimental conditions insulin enhances the equilibrating glucose entry by the phloretin-sensitive pathway at the basal-lateral membrane, and transiently inhibits the Na-glucose cotransport system.
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PMID:Glucose transport and metabolism in rat renal proximal tubules: multicomponent effects of insulin. 293 29


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